松田　覚MATSUDA Satoruマツダ　サトル

researchmap

プロフィール情報

• 姓

  松田, マツダ

• 名

  覚, サトル

学位

• 医学博士, 東京大学

研究分野

• ライフサイエンス, 医化学

経歴

• 2003年10月, 奈良女子大学生活環境学部教授
• 2000年04月, 2003年09月, 名古屋大学医学部助教授
• 1997年07月, 2000年03月, 名古屋大学医学部講師
• 1992年04月, 1997年06月, 東京大学医科学研究所助手
• 1990年04月, 1992年03月, 学術振興会特別研究員

学歴

• 1988年, 東京大学大学院, 医学系研究科, 第一臨床医学

担当経験のある科目（授業）

• 分子食医化学演習, 奈良女子大学
• 食品貯蔵学, 奈良女子大学
• 病態内科学, 奈良女子大学
• キャリアデザイン・ゼミナールA（３３）, 奈良女子大学
• キャリアデザイン・ゼミナールＡ（１３）, 奈良女子大学
• キャリアデザイン・ゼミナールＡ（１２）, 奈良女子大学
• 分子食医化学, 奈良女子大学
• 臨床栄養学総論, 奈良女子大学
• キャリアデザイン・ゼミナールA（３２）, 奈良女子大学
• キャリアデザイン・ゼミナールＡ（２３）, 奈良女子大学
• キャリアデザイン・ゼミナールＡ（１１）, 奈良女子大学
• 病態生理・生化学実験, 奈良女子大学
• 分子生活習慣病論演習, 奈良女子大学
• 食医化学演習, 奈良女子大学
• 食品生物工学, 奈良女子大学
• 分子生活習慣病論, 奈良女子大学
• 食医化学, 奈良女子大学
• 基礎栄養学実験, 奈良女子大学
• 生化学Ⅰ, 奈良女子大学

所属学協会

• 日本分子生物学会
• 日本生化学会
• 日本癌学会
• 日本家政学会

Ⅱ．研究活動実績

論文

• 査読あり, 英語, Diseases (Basel, Switzerland), Roles of PI3K/AKT/GSK3 Pathway Involved in Psychiatric Illnesses., 辻愛; 松田覚, Psychiatric illnesses may be qualified to the cellular impairments of the function for survival or death in neurons, which may consequently appear as abnormalities in the neuroplasticity. The molecular mechanism has not been well understood, however, it seems that PI3K, AKT, GSK3, and their downstream molecules have crucial roles in the pathogenesis. Through transducing cell surviving signal, the PI3K/AKT/GSK3 pathway may organize an intracellular central network for the action of the synaptic neuroplasticity. In addition, the pathways may also regulate cell proliferation, cell migration, and apoptosis. Several lines of evidence have supported a role for this signaling network underlying the development and treatment for psychiatric illnesses. Indeed, the discovery of molecular biochemical phenotypes would represent a breakthrough in the research for effective treatment. In this review, we summarize advances on the involvement of the PI3K/AKT/GSK3 pathways in cell signaling of neuronal cells. This study may provide novel insights on the mechanism of mental disorder involved in psychiatric illnesses and would open future opportunity for contributions suggesting new targets for diagnostic and/or therapeutic procedures., 2019年02月13日, 7, 1, 研究論文（学術雑誌）, 国際誌, 10.3390/diseases7010022
• 査読あり, 英語, Neural regeneration research, By using either endogenous or transplanted stem cells, which could you prefer for neural regeneration?, 辻愛; 松田覚, 2018年10月, 13, 10, 1731, 1732, 研究論文（学術雑誌）, 国際誌, 10.4103/1673-5374.238609
• 査読あり, 英語, Diseases (Basel, Switzerland), Implications of PI3K/AKT/PTEN Signaling on Superoxide Dismutases Expression and in the Pathogenesis of Alzheimer's Disease., 辻愛, 松田覚, Alzheimer’s disease is a neurodegenerative sickness, where the speed of personal disease progression differs prominently due to genetic and environmental factors such as life style. Alzheimer’s disease is described by the construction of neuronal plaques and neurofibrillary tangles composed of phosphorylated tau protein. Mitochondrial dysfunction may be a noticeable feature of Alzheimer’s disease and increased production of reactive oxygen species has long been described. Superoxide dismutases (SODs) protect from excess reactive oxygen species to form less reactive hydrogen peroxide. It is suggested that SODs can play a protective role in neurodegeneration. In addition, PI3K/AKT pathway has been shown to play a critical role on the neuroprotection and inhibiting apoptosis via the enhancing expression of the SODs. This pathway appears to be crucial in Alzheimer’s disease because it is related to the tau protein hyper-phosphorylation. Dietary supplementation of several ordinary compounds may provide a novel therapeutic approach to brain disorders by modulating the function of the PI3K/AKT pathway. Understanding these systems may offer a better efficacy of new therapeutic approaches. In this review, we summarize recent progresses on the involvement of the SODs and PI3K/AKT pathway in neuroprotective signaling against Alzheimer’s disease., 2018年04月20日, 6, 2, 研究論文（学術雑誌）, 国際誌, 10.3390/diseases6020028
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, PI3K/AKT signaling mediated by G protein-coupled receptors is involved in neurodegenerative Parkinson's disease, Noriko Nakano; Satoru Matsuda; Mayuko Ichimura; Akari Minami; Mako Ogino; Toshiyuki Murai; Yasuko Kitagishi, Parkinson's disease (PD) is a common progressive and multifactorial neurodegenerative disease, characterized by the loss of midbrain dopaminergic neurons. Numerous pathological processes including, inflammation, oxidative stress, mitochondrial dysfunction, neurotransmitter imbalance, and apoptosis as well as genetic factors may lead to neuronal degeneration. Motor deficits in PD are due mostly to the progressive loss of nigrostriatal dopaminergic neurons. Neuroprotection of functional neurons is of significance in the treatment of PD. G protein-coupled receptors (GPCRs) have been implicated in the neuroprotection against PD through the survival of dopaminergic neurons. In addition, phosphatidyl-inositol-3-kinase (PI3K)/AKT signaling has also been demonstrated to be neuroprotective. Knowledge of the mechanisms involved in this cellular protection could be critical for developing treatments to prevent this neurodegenerative disorder. In this review, we highlight the protective roles of the PI3K/AKT signaling pathway in the function of representative serotonin GPCRs. Particular attention is given to the molecular mechanisms of this pathway proposed to explain the favorable effects of food ingredients against neurodegenerative disease., 2017年02月, 39, 2, 253, 260, 10.3892/ijmm.2016.2833
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, Roles of oncogenes and tumor-suppressor genes in osteoclastogenesis, Akari Minami; Mako Ogino; Noriko Nakano; Mayuko Ichimura; Atsuko Nakanishi; Toshiyuki Murai; Yasuko Kitagishi; Satoru Matsuda, Osteoporosis is a bone disease that poses a tremendous burden to health care. The receptor activator of nuclear factor-KB (RANK) and its ligand (RANKL) have been a major focus of this research field. RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also adjusts bone homeostasis both in normal physiology and in bone disease. Consequently, novel drugs specifically targeting RANK-RANKL and their signaling pathways in osteoclasts are expected to revolutionize the treatment of various bone diseases such as osteoporosis. Osteoclasts are the exclusive cells involved in bone resorption. Abnormal activation of osteoclasts can lead to reduced bone density, resulting in osteopenia, osteoporosis and other bone disorders. To date, the mechanism of how osteoclast precursors differentiate into mature osteoclasts remains elusive. Cell proliferation and cell death may be key processes in the progression as well as other cell types. Oncogene products and tumor-suppressor molecules play a pivotal role in regulating the processes, which are important in regulating the configuration of bone disorders. Based on the understanding of these processes, promising alternatives to the use of medications against osteoporosis include specific diets with plant-derived supplements to modulate the expression and/or activity of these molecules. In this review, we summarize the progress of research with a focus on the modulatory roles of oncogene products and tumor-suppressor molecules and suggest the scope of further research concerning the prevention of osteoporosis in this field., 2017年02月, 39, 2, 261, 267, 10.3892/ijmm.2017.2847
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, PINK1 signaling in mitochondrial homeostasis and in aging (Review), Yasuko Kitagishi; Noriko Nakano; Mako Ogino; Mayuko Ichimura; Akari Minami; Satoru Matsuda, Mitochondrial dysfunction is involved in the pathology of Parkinson's disease, an age-associated neurodegenerative disorder. Phosphatase and tensin homolog (PTEN)-induced putative kinase protein 1 (PINK1) is responsible for the most common form of recessive Parkinson's disease. PINK1 is a mitochondrial kinase that is involved in mitrochondrial quality control and promotes cell survival. PINK1 has been shown to protect against neuronal cell death induced by oxidative stress. Accordingly, PINK1 deficiency is associated with mitochondrial dysfunction as well as increased oxidative cellular stress and subsequent neuronal cell death. In addition, several mitochondrial chaperone proteins have been shown to be substrates of the PINK1 kinase. In this review, we discuss recent studies concerning the signaling cascades and molecular mechanisms involved in the process of mitophagy, which is implicated in neurodegeneration and in related aging associated with oxidative stress. Particular attention will be given to the molecular mechanisms proposed to explain the effects of natural compounds and/or food ingredients against oxidative stress. Knowledge of the molecular mechanisms involved in this cellular protection could be critical for developing treatments to prevent and control excessive progression of neurodegenerative disorders., 2017年01月, 39, 1, 3, 8, 10.3892/ijmm.2016.2827
• 査読あり, 英語, INTERNATIONAL JOURNAL OF ONCOLOGY, Effective PI3K modulators for improved therapy against malignant tumors and for neuroprotection of brain damage after tumor therapy (Review), Satoru Matsuda; Mayuko Ichimura; Mako Ogino; Noriko Nakano; Akari Minami; Toshiyuki Murai; Yasuko Kitagishi, Due to the key role in various cellular processes including cell proliferation and cell survival on many cell types, dysregulation of the PI3K/AKT pathway represents a crucial step of the pathogenesis in many diseases. Furthermore, the tumor suppressor PTEN negatively regulates the PI3K/AKT pathway through its lipid phosphatase activity, which is recognized as one of the most frequently deleted and/or mutated genes in human cancer. Given the pervasive involvement of this pathway, the development of the molecules that modulate this PI3K/AKT signaling has been initiated in studies which focus on the extensive effective drug discovery. Consequently, the PI3K/AKT pathway appears to be an attractive pharmacological target both for cancer therapy and for neurological protection necessary after the therapy. A better understanding of the molecular relations could reveal new targets for treatment development. We review recent studies on the features of PI3K/AKT and PTEN, and their pleiotropic functions relevant to the signaling pathways involved in cancer progress and in neuronal damage by the therapy., 2016年11月, 49, 5, 1785, 1790, 10.3892/ijo.2016.3710
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, Roles of PTEN with DNA Repair in Parkinson's Disease, Mako Ogino; Mayuko Ichimura; Noriko Nakano; Akari Minami; Yasuko Kitagishi; Satoru Matsuda, Oxidative stress is considered to play key roles in aging and pathogenesis of many neurodegenerative diseases such as Parkinson's disease, which could bring DNA damage by cells. The DNA damage may lead to the cell apoptosis, which could contribute to the degeneration of neuronal tissues. Recent evidence suggests that PTEN (phosphatase and tensin homolog on chromosome 10) may be involved in the pathophysiology of the neurodegenerative disorders. Since PTEN expression appears to be one dominant determinant of the neuronal cell death, PTEN should be a potential molecular target of novel therapeutic strategies against Parkinson's disease. In addition, defects in DNA damage response and DNA repair are often associated with modulation of hormone signaling pathways. Especially, many observations imply a role for estrogen in a regulation of the DNA repair action. In the present review, we have attempted to summarize the function of DNA repair molecules at a viewpoint of the PTEN signaling pathway and the hormone related functional modulation of cells, providing a broad interpretation on the molecular mechanisms for treatment of Parkinson's disease. Particular attention will be paid to the mechanisms proposed to explain the health effects of food ingredients against Parkinson's disease related to reduce oxidative stress for an efficient therapeutic intervention., 2016年06月, 17, 6, E954, 10.3390/ijms17060954
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, BRCA1 and p53 Tumor Suppressor Molecules in Alzheimer's Disease, Atsuko Nakanishi; Akari Minami; Yasuko Kitagishi; Yasunori Ogura; Satoru Matsuda, Tumor suppressor molecules play a pivotal role in regulating DNA repair, cell proliferation, and cell death, which are also important processes in the pathogenesis of Alzheimer's disease. Alzheimer's disease is the most common neurodegenerative disorder, however, the precise molecular events that control the death of neuronal cells are unclear. Recently, a fundamental role for tumor suppressor molecules in regulating neurons in Alzheimer's disease was highlighted. Generally, onset of neurodegenerative diseases including Alzheimer's disease may be delayed with use of dietary neuro-protective agents against oxidative stresses. Studies suggest that dietary antioxidants are also beneficial for brain health in reducing disease-risk and in slowing down disease-progression. We summarize research advances in dietary regulation for the treatment of Alzheimer's disease with a focus on its modulatory roles in BRCA1 and p53 tumor suppressor expression, in support of further therapeutic research in this field., 2015年02月, 16, 2, 2879, 2892, 10.3390/ijms16022879
• 査読あり, 英語, FRONTIERS IN BIOSCIENCE-LANDMARK, Functions and characteristics of PINK1 and Parkin in cancer, Satoru Matsuda; Atsuko Nakanishi; Akari Minami; Yoko Wada; Yasuko Kitagishi, Most of the Parkinson disease (PD) linked genes are also associated with cancers. In particular, phosphatase and tensin homologue-induced kinase 1 (PINK1) and Parkin, both of which are involved in recessively inherited familial forms of PD linked to mitochondrial dysfunction, appear to be abnormally expressed in cancers. Functional studies have revealed that PINK1 recruits Parkin to mitochondria to initiate mitophagy, an important autophagic quality control mechanism that rids the cell of damaged mitochondria. Although PD and cancer are obviously disparate human disorders, there is an evidence for low cancer rates in patients with PD. The relationship between cancer rates and PD might be related to the involvement of common pathways in both diseases. This paper provides a concise overview on the cellular functions of the PINK1 and Parkin., 2015年01月, 20, 491, 501, 研究論文（学術雑誌）, 10.2741/4321
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, Function of α-synuclein and PINK1 in Lewy body dementia, 松田覚, alpha-synuclein (-syn) is the major protein component of Lewy bodies, a key pathological characteristic of the degenerating brain. The misfolding and aggregation of -syn is associated with both the idiopathic and familial forms of Parkinson's disease (PD) and Lewy body dementia (LBD). However, the function of -syn is poorly understood, as it shows both neurotoxic and neuroprotective activities. Mutations in phosphatase and tensin homologue-induced putative kinase 1 (PINK1) also cause recessively inherited PD. Studies support the notion of neuroprotective roles for PINK1, as it protects cells from damage-induced mitochondrial dysfunction, oxidative stress and cell apoptosis. PINK1 plays an essential role in mitochondrial quality control and its homeostasis is maintained through mitochondrial stabilization. The -syn aggregation is linked to various aspects of mitochondrial dysfunction and PINK1-related mitophagy. Determination of the molecular pathways that lead to -syn oligomerization and further aggregation may be the basis for the successful design and development of treatments for these neurodegenerative diseases. The present review summarizes the function of PINK1 underlying -syn aggregation and the mechanisms through which mitochondrial dysfunction plays a role in this process., 2015年01月, 35, 1, 3, 9, 研究論文（学術雑誌）, 10.3892/ijmm.2014.1980
• 査読あり, 英語, Open Biochem J, Certain Diet and Lifestyle May Contribute to Islet β-cells Protection in Type-2 Diabetes via the Modulation of Cellular PI3K/AKT Pathway., 松田覚, 2014年11月, 8, 74-82, 10.2174/1874091X01408010074
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, Atherosclerosis and tumor suppressor molecules (Review), Miho Suzuki; Aicari Minami; Atsuko Nakanishi; Keiko Kobayashi; Satoru Matsuda; Yasunori Ogura; Yasuko Kitagishi, Atherosclerosis, the major cause of heart attack and stroke, is a chronic inflammatory disease characterized by the formation of atherosclerotic plaque. Oxidized low-density lipoprotein through increased oxidative stress has been identified as one of the primary factors responsible for atherogenesis. Cell proliferation and death are key processes in the progression of atherosclerosis. The oxidative environment in areas of lipid accumulation is mainly created by the production of reactive oxygen species, which are assumed to mediate vascular tissue injury. Oxidative DNA damage and levels of DNA repair are reduced during dietary lipid lowering. The tumor suppressor molecules play a pivotal role in regulating cell proliferation, DNA repair and cell death, which are important processes in regulating the composition of atherosclerotic plaque. Accordingly, in this review, we discuss the fundamental role of tumor suppressor molecules in regulating atherogenesis. In particular, we discuss how tumor suppressor molecules are activated in the complex environment of atherosclerotic plaque, and regulate growth arrest, cell senescence and the apoptosis of vascular smooth muscle cells, which may protect against the progression of atherosclerosis. In addition, we discuss promising alternatives to the use of medications (such as statin) against atherosclerosis, namely diet, with the use of plant-derived supplements to modulate the expression and/or activity of tumor suppressor molecules. We also summarize the progress of research made on herbs with a focus on the modulatory roles of tumor suppressors, and on the molecular mechanisms underlying the prevention if atherosclerosis, supporting designs for further research in this field., 2014年10月, 34, 4, 934, 940, 研究論文（学術雑誌）, 10.3892/ijmm.2014.1866
• 査読あり, 英語, INTERNATIONAL JOURNAL OF ONCOLOGY, The tumor suppressor PTEN interacts with p53 in hereditary cancer (Review), Atsuko Nakanishi; Yasuko Kitagishi; Yasunori Ogura; Satoru Matsuda, Numerous hereditary syndromes caused by mutations in multiple tumor suppressor genes can cause cancers. Germ line mutations in PTEN and p53 tumor suppressor cause Cowden syndrome and Li-Fraumeni syndrome, respectively. There exists some phenotypic overlap in these syndromes, and they are associated with high risks of breast cancer. The tumor suppressor protein PTEN is a dual-specificity phosphatase which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI3K activity. Cells that lack PTEN have constitutively higher levels of PIP3 and activated downstream targets. PTEN gene is recognized as one of the most frequently mutated or mutated in many human cancers. Li-Fraumeni syndrome results from germline mutations of the tumor suppressor p53 gene encoding a transcriptional factor able to regulate cell cycle and apoptosis when DNA damage occurs. The p53 protein cooperates with PTEN and might be an essential blockage in development of mammary tumors. Many findings have demonstrated that PTEN as well as p53 plays a critical role in DNA damage response. This review summarizes the function of PTEN and p53 in carcinogenic cell signaling. In addition, we will discuss the role of PTEN signaling through its interaction with p53 and MDM2 pathways for the potential implications in hereditary cancer prevention and therapeutic intervention., 2014年06月, 44, 6, 1813, 1819, 10.3892/ijo.2014.2377
• 査読あり, 英語, AGING AND DISEASE, Link between PI3K/AKT/PTEN Pathway and NOX Protein in Diseases, Atsuko Nakanishi; Yoko Wada; Yasuko Kitagishi; Satoru Matsuda, Accumulating evidence has revealed that the PI3K/AKT/PTEN pathway acts as a pivotal determinant of cell fate regarding senescence and apoptosis, which is mediated by intracellular reactive oxygen species (ROS) generation. NADPH oxidase (NOX) family of enzymes generates the ROS. The regulation of NOX enzymes is complex, with many members of this family exhibiting complexity in terms of subunit composition, cellular location, and tissue-specific expression. Cells are continuously exposed to the ROS, which represent mutagens and are thought to be a major contributor to several diseases including cancer and aging process. Therefore, cellular ROS sensing and metabolism are firmly regulated by a variety of proteins involved in the redox mechanism. In this review, the roles of oxidative stress in PI3K/AKT/PTEN signaling are summarized with a focus on the links between the pathways and NOX protein in several diseases including cancer and aging., 2014年06月, 5, 3, 203, 211, 10.14336/AD.2014.0500203
• 査読あり, 英語, ALZHEIMERS RESEARCH & THERAPY, Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer's disease., 松田覚, Alzheimer's disease (AD) is characterized by the formation of senile plaques and neurofibrillary tangles composed of phosphorylated Tau. Several findings suggest that correcting signal dysregulation for Tau phosphorylation in AD may offer a potential therapeutic approach. The PI3K/AKT/GSK-3 beta pathway has been shown to play a pivotal role in neuroprotection, enhancing cell survival by stimulating cell proliferation and inhibiting apoptosis. This pathway appears to be crucial in AD because it promotes protein hyper-phosphorylation in Tau. Understanding those regulations may provide a better efficacy of new therapeutic approaches. In this review, we summarize advances in the involvement of the PI3K/AKT/GSK-3 beta pathways in cell signaling of neuronal cells. We also review recent studies on the features of several diets and the signaling pathway involved in AD., 2014年, 6, 3, 35, 10.1186/alzrt265
• 査読あり, 英語, Frontiers in Oncology, Connection between tumor suppressor BRCA1 and PTEN in damaged DNA repair, Akari Minami; Atsuko Nakanishi; Yasunori Ogura; Yasuko Kitagishi; Satoru Matsuda, Genomic instability finally induces cell death or apoptosis. The tumor suppressor, phosphatase and tensin homolog on chromosome 10 (PTEN), is a dual-specificity phosphatase, which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI3K activity. Cells that lack PTEN have constitutively higher levels of PIP3 and activated downstream PI3K/AKT targets. BRCA1, a well-known breast cancer tumor suppressor, is to associate with breast cancer risk and genetic susceptibility. Many studies have demonstrated that PTEN, as well as BRCA1, plays a critical role in DNA damage responses. The BRCA1 functionally cooperates with PTEN and might be an essential blockage in the development of several tumors. Actually, the PTEN and BRCA1 genes are recognized as one of the most frequently deleted and/or mutated in many human cancers. The PI3K/AKT pathway is constitutively active in BRCA1-defective human cancer cells. Loss or decrease of these PTEN or BRCA1 function, by either mutation or reduced expression, has a role in various tumor developments. This review summarizes recent findings of the function of BRCA1 and PTEN involved in genomic stability and cancer cell signaling., 2014年, 4, 318, 10.3389/fonc.2014.00318
• 査読あり, 英語, International Journal of Molecular Sciences, RUFY, rab and rap family proteins involved in a regulation of cell polarity and membrane trafficking, Yasuko Kitagishi; Satoru Matsuda, Cell survival, homeostasis and cell polarity rely on the control of membrane trafficking pathways. The RUN domain (comprised of the RPIP8, UNC-14, and NESCA proteins) has been suggested to be implicated in small GTPase-mediated membrane trafficking and cell polarity. Accumulating evidence supports the hypothesis that the RUN domain-containing proteins might be responsible for an interaction with a filamentous network linked to actin cytoskeleton and/or microtubules. In addition, several downstream molecules of PI3K are involved in regulation of the membrane trafficking by interacting with vesicle-associated RUN proteins such as RUFY family proteins. In this review, we summarize the background of RUN domain research with an emphasis on the interaction between RUN domain proteins including RUFY proteins (designated as RUN and FYVE domain-containing proteins) and several small GTPases with respect to the regulation of cell polarity and membrane trafficking on filamentous network. © 2013 by the authors licensee MDPI, Basel, Switzerland., 2013年03月, 14, 3, 6487, 6498, 10.3390/ijms14036487
• 査読あり, 英語, Int J Mol Med, Redox regulation of tumor suppressor PTEN in cancer and aging, 松田覚, 2013年01月, 31, 3, 511
• 査読あり, 英語, ISRN Endocrinol, Roles for PI3K/AKT/PTEN Pathway in Cell Signaling of Nonalcoholic Fatty Liver Disease., 松田覚, 2013年01月, 3013, 472432
• 査読あり, 英語, PPAR Research, Expression and function of PPARs in placenta, Satoru Matsuda; Mayumi Kobayashi; Yasuko Kitagishi, Peroxisome proliferator-activated receptors (PPAR) are members of the superfamily of nuclear hormone receptors involved in embryonic development and differentiation of several tissues including placenta, which respond to specific ligands such as polyunsaturated fatty acids by altering gene expression. Three subtypes of this receptor have been discovered, each evolving to achieve different biological functions. The PPARs also control a variety of target genes involved in lipid homeostasis. Similar to other nuclear receptors, the transcriptional activity of PPARs is affected not only by ligand-stimulation but also by crosstalk with other molecules. For example, both PPARs and the RXRs are ligand-activated transcription factors that coordinately regulate gene expression. In addition, several mechanisms underlying negative regulation of gene expression by PPARs have been shown. It is suggested that PPARs are key messengers responsible for the translation of nutritional stimuli into changes in gene expression pathways for placental development. © 2013 Satoru Matsuda et al., 2013年, 2013, 256508, 10.1155/2013/256508
• 査読あり, 英語, OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, Function and Characteristics of PINK1 in Mitochondria, Satoru Matsuda; Yasuko Kitagishi; Mayumi Kobayashi, Mutations in phosphatase and tensin homologue-induced kinase 1 (PINK1) cause recessively inherited Parkinson's disease, a neurodegenerative disorder linked to mitochondrial dysfunction. Studies support the notion of neuroprotective roles for the PINK1, as it protects cells from damage-mediated mitochondrial dysfunction, oxidative stress, and cell apoptosis. PARL is a mitochondrial resident rhomboid serine protease, and it has been reported to mediate the cleavage of the PINK1. Interestingly, impaired mitophagy, an important autophagic quality control mechanism that clears the cells of damaged mitochondria, may also be an underlying mechanism of disease pathogenesis in patients for Parkinson's disease with the PARL mutations. Functional studies have revealed that PINK1 recruits Parkin to mitochondria to initiate the mitophagy. PINK1 is posttranslationally processed, whose level is definitely regulated in healthy steady state of mitochondria. As a consequence, PINK1 plays a pivotal role in mitochondrial healthy homeostasis., 2013年, 2013, 601587, 10.1155/2013/601587
• 査読あり, 英語, ALZHEIMERS RESEARCH & THERAPY, Diets involved in PPAR and PI3K/AKT/PTEN pathway may contribute to neuroprotection in a traumatic brain injury, Yasuko Kitagishi; Satoru Matsuda, Traumatic encephalopathy has emerged as a significant public health problem. It is believed that traumatic encephalopathy is caused by exposure to repetitive brain trauma prior to the initial symptoms of neurodegenerative disease. Therefore, prevention is important for the disease. The PI3K/AKT/PTEN (phosphoinositide-3 kinase/AKT/phosphatase and tensin homologue deleted on chromosome 10) pathway has been shown to play a pivotal role in neuroprotection, enhancing cell survival by stimulating cell proliferation and inhibiting apoptosis. PTEN negatively regulates the PI3K/AKT pathways through its lipid phosphatase activity. Although PTEN has been discovered as a tumor suppressor, PTEN is also involved in several other diseases, including diabetes and Alzheimer's disease. Dietary fish oil rich in polyunsaturated fatty acids may induce the PTEN expression by activation of peroxisome proliferator-activated receptor. Supplementation of these natural compounds may provide a new therapeutic approach to the brain disorder. We review recent studies on the features of several diets and the signaling pathways involved in traumatic encephalopathy., 2013年, 5, 5, 42, 10.1186/1758-9193-5-42
• 査読あり, 英語, Cancers, Peroxisome proliferator-activated receptor and vitamin D receptor signaling pathways in cancer cells, Satoru Matsuda; Yasuko Kitagishi, Peroxisome proliferator-activated receptors (PPARs) are members of the superfamily of nuclear hormone receptors, which respond to specific ligands such as polyunsaturated fatty acids by altering gene expression. Three subtypes of this receptor have been discovered, each evolving to achieve different biological functions. Like other nuclear receptors, the transcriptional activity of PPARs is affected not only by ligand-stimulation, but also by cross-talk with other molecules. For example, both PPARs and the RXRs are ligand-activated transcription factors that coordinately regulate gene expression. In addition, PPARs and vitamin D receptor (VDR) signaling pathways regulate a multitude of genes that are of importance for cellular functions including cell proliferation and cell differentiation. Interaction of the PPARs and VDR signaling pathways has been shown at the level of molecular cross-regulation of their transcription factor. A variety of ligands influencing the PPARs and VDR signaling pathways have been shown to reveal chemopreventive potential by mediating tumor suppressive activities in human cancers. Use of these compounds may represent a potential novel strategy to prevent cancers. This review summarizes the roles of the PPARs and the VDR in pathogenesis and progression of cancer., 2013年, 5, 4, 1261, 1270, 10.3390/cancers5041261
• 査読あり, 英語, Open Medicinal Chemistry Journal, Roles of PI3K/AKT/PTEN pathway as a target for Pharmaceutical therapy, Satoru Matsuda; Atsuko Nakanishi; Yoko Wada; Yasuko Kitagishi, Multiple enzymes participate in the phosphorylation of a group of phosphoinositide lipids. Because of their important role in signal transduction, the dysregulated metabolism of phosphoinositides represents a key step in many disease settings. Loss of their function has been demonstrated to occur as an early event a wide variety of carcinogenesis and has therefore been suggested as a biomarker for the premalignant disease. In addition, genetic alterations at multiple nodes in the pathway have been implicated in several other diseases. Accordingly, given this pervasive involvement in many diseases, the development of molecules that modulates this pathway has been initiated in studies. They have been the focus of extensive research and drug discovery activities. A better understanding of the molecular connections could uncover new targets for drug development. © Matsuda et al., 2013年, 7, 1, 23, 29, 研究論文（学術雑誌）, 10.2174/1874104501307010023
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, Elucidating the regulation of T cell subsets (Review), Yasuko Kitagishi; Mayumi Kobayashi; Yurie Yamashina; Satoru Matsuda, CD4-positive T lymphocytes mainly direct immune as well as autoimmune responses against a variety of pathogens or allergens. This is achieved through the acquisition of specialized functions followed by differentiation into various T cell subsets. The differentiation process of naive T cells into effector subsets is regulated by dendritic cells and secreted cytokines. Signal transducer and activator of transcription proteins play critical roles in transmitting cytokine-mediated signals and specifying T cell differentiation. Epigenetic changes such as historic acetylation and methylation along with DNA methylation also regulate expression of differentiation-specific genes. Defining, exactly how extrinsic signals control the specification of T cells will provide important insights and therapeutic opportunities., 2012年12月, 30, 6, 1255, 1260, 研究論文（学術雑誌）, 10.3892/ijmm.2012.1152
• 査読あり, 英語, ONCOLOGY LETTERS, Terpinolene, a component of herbal sage, downregulates AKT1 expression in K562 cells, Naoko Okumura; Hitomi Yoshida; Yuri Nishimura; Yasuko Kitagishi; Satoru Matsuda, Protein kinase AKT mediates cell proliferation and survival signals, and also contributes to cancer progression. Increased expression and/or activation of AKT is involved in a variety of human cancers. In cells treated with sage or rosemary extract, mRNA and protein expression levels of AKT1 were reduced compared with those of the control cells 48 h after the herbal treatments. We found that terpinolene, a common component of sage and rosemary, markedly reduced the protein expression of AKT1 in K562 cells and inhibited cell proliferation., 2012年02月, 3, 2, 321, 324, 研究論文（学術雑誌）, 10.3892/ol.2011.491
• 査読あり, 英語, MOLECULAR MEDICINE REPORTS, Clobetasol synergistically diminishes Ciz1 expression with genistein in U937 cells, Naoko Okumura; Hitomi Yoshida; Yuri Nishimura; Yasuko Kitagishi; Satoru Matsuda, Cip-interacting zinc finger protein 1 (Ciz1) stimulates DNA replication and has been implicated in the tumorigenesis of breast cancer cells. In order to investigate the possibility of using medicinal glucocorticoids against breast cancer, we studied whether certain glucocorticoids affect the expression of Ciz1. The in vitro effect of clobetasol treatment on the reduction of Ciz1 expression was detected by reverse transcriptase-polymerase chain reaction. Western blotting also confirmed the down-regulation of the protein in a dose-dependent manner upon clobetasol treatment in U937 monocytoid cells. Furthermore, we found that Ciz1 protein expression was decreased after pre-treatment of the cells with clobetasol and genistein. An extract of Lens culinaris also had a synergistic effect on the repression of Ciz1 protein expression., 2012年02月, 5, 2, 567, 569, 研究論文（学術雑誌）, 10.3892/mmr.2011.665
• 査読あり, 英語, MOLECULAR MEDICINE REPORTS, Genistein downregulates presenilin 1 and ubiquilin 1 expression, Naoko Okumura; Hitomi Yoshida; Yuri Nishimura; Mutsumi Murakami; Yasuko Kitagishi; Satoru Matsuda, The aim of this study was to determine the effects of several food ingredients and chemical inhibitors on the expression of presenilin, a molecule involved in gamma-secretase activity and the generation of amyloid-beta peptide in Alzheimer's disease. Western blotting revealed the downregulation of presenilin 1 protein expression by stimulation with genistein in vitro, while the effects on presenilin 1 gene expression examined by reverse transcriptase-polymerase chain reaction (RT-PCR) were unaltered in Daudi cells. Genistein likely downregulates presenilin via the inhibition of ubiquilin 1 expression in lymphoid cells. Our findings provide new insights that may help to establish preventive strategies against Alzheimer's disease., 2012年02月, 5, 2, 559, 561, 研究論文（学術雑誌）, 10.3892/mmr.2011.648
• 査読あり, 英語, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, Clobetasol down-regulates SLPI expression in U937 monocytoid cells, Naoko Okumura; Hitomi Yoshida; Yasuko Kitagishi; Yuri Nishimura; Satoru Matsuda, In order to investigate how glucocorticoids affect the expression of secretory leukocyte peptidase inhibitor (SLPI), which is overexpressed in a variety of cancers, clobetasol was added to cell culture medium of U937 cells and the SLPI mRNA levels were examined. The in vitro effect of the treatment on SLPI expression was detected by reverse transcriptase-polymerase chain reaction. Clobetasol treatment of U937 cells induced an up- and down-regulation of SLPI expression in a dose-dependent manner. Western blotting confirmed the down-regulation of SLPI protein expression. We hypothesized a loop formation in the SLPI genome domain, in which the glucocorticoid receptor regulates bi-directional transcriptional activity., 2012年02月, 29, 2, 324, 326, 研究論文（学術雑誌）
• 査読あり, 英語, Advances in Hematology, PI3K/AKT/PTEN signaling as a molecular target in leukemia angiogenesis, Naoko Okumura; Hitomi Yoshida; Yasuko Kitagishi; Mutsumi Murakami; Yuri Nishimura; Satoru Matsuda, PI3K/AKT/PTEN pathway is important in the regulation of angiogenesis mediated by vascular endothelial growth factor in many tumors including leukemia. The signaling pathway is activated in leukemia patients as well as leukemia cell lines together with a decrease in the expression of PTEN gene. The mechanism by which the signaling pathway regulates angiogenesis remains to be further elucidated. However, it has become an attractive target for drug therapy against leukemia, because angiogenesis is a key process in malignant cell growth. In this paper, we will focus on the roles and mechanisms of PI3K/AKT/PTEN pathway in regulating angiogenesis. © 2012 Naoko Okumura et al., 2012年, 2012, 843085, 10.1155/2012/843085
• 査読あり, 英語, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Alternative splicings on p53, BRCA1 and PTEN genes involved in breast cancer, Naoko Okumura; Hitomi Yoshida; Yasuko Kitagishi; Yuri Nishimura; Satoru Matsuda, Alternative splicing is a major contributor to transcriptome and proteome diversity, which can lead to the deregulation of crucial cellular processes and have been associated with a variety of human diseases including cancer. As p53, BRCA1, and PTEN proteins have a key role in preventing breast cancer formation, cancer-associated splicing variants of these tumor suppressor genes are potential molecular markers and may contribute to the development of diagnostic and prognostic methods. In the present review, we summarize these tumor suppressor genes at a viewpoint of alternative splicing involved in breast cancer. (C) 2011 Elsevier Inc. All rights reserved., 2011年09月, 413, 3, 395, 399, 10.1016/j.bbrc.2011.08.098
• 査読あり, 英語, IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, Long-term cultivation of in vitro Apis mellifera cells by gene transfer of human c-myc proto-oncogene, Yasuko Kitagishi; Naoko Okumura; Hitomi Yoshida; Yuri Nishimura; Jun-ichi Takahashi; Satoru Matsuda, Establishment of cell lines representative of honeybee character would greatly assist in their analysis. Here, we show that immortalized cell line, designated as MYN9, has been generated from honeybee embryo by the gene transfer of human c-myc proto-oncogene. The morphology of the cell is characteristic of embryonic stem cell, although the cell is stable and does not spontaneously differentiate. Polymerase chain reaction analyses show that the cell is originated from authentic honeybee cell. It is proposed that the integration of human c-myc gene into honeybee precursor populations results in the establishment of stable cell line suitable for cellular and molecular studies., 2011年08月, 47, 7, 451, 453, 研究論文（学術雑誌）, 10.1007/s11626-011-9431-6
• 査読あり, 英語, MOLECULAR MEDICINE REPORTS, Ethanol extracts of black pepper or turmeric down-regulated SIRT1 protein expression in Daudi culture cells, Yuri Nishimura; Yasuko Kitagishi; Hitomi Yoshida; Naoko Okumura; Satoru Matsuda, SIRT1 is a mammalian candidate molecule involved in longevity and diverse metabolic processes. The present study aimed to determine the effects of certain herbs and spices on SIRT1 expression. Human cell lines Daudi, Jurkat, U937 and K562 were cultured in RPMI-1640. Herb and spice powders were prepared and the supernatants were collected. RT-PCR was used to quantify the expression level of the gene. Protein samples were then analyzed by Western blotting. Western blotting revealed the down-regulation of SIRT1 protein expression in Daudi cells treated with extracts of black pepper or turmeric. On the other hand, the effect on the SIRT1 gene expression examined by reverse transcription polymerase chain reaction was unaltered. In conclusion, component(s) of certain herbs and spices may induce the down-regulation of SIRT1 protein., 2011年07月, 4, 4, 727, 730, 研究論文（学術雑誌）, 10.3892/mmr.2011.487
• 査読あり, 英語, EXPERIMENTAL AND THERAPEUTIC MEDICINE, Turmeric and curcumin suppress presenilin 1 protein expression in Jurkat cells, Hitomi Yoshida; Naoko Okumura; Yuri Nishimura; Yasuko Kitagishi; Satoru Matsuda, In the present study, we aimed to determine the effects of herbs or spices on the expression of presenilin 1, a molecule involved in gamma-secretase activity and the generation of amyloid-beta peptide in Alzheimer's disease. Western blot analysis revealed that presenilin 1 protein expression was down-regulated by stimulation with turmeric or cinnamon extracts in vitro, while the effects on presenilin 1 gene expression examined by reverse transcriptase-polymerase chain reaction were unaltered. Our results showed that curcumin, a component of turmeric, induced the down-regulation of presenilin 1 protein in Jurkat and K562 cell lines., 2011年07月, 2, 4, 629, 632, 研究論文（学術雑誌）, 10.3892/etm.2011.246
• 査読あり, 英語, FEBS LETTERS, How do you RUN on?, Hitomi Yoshida; Yasuko Kitagishi; Naoko Okumura; Mutsumi Murakami; Yuri Nishimura; Satoru Matsuda, RUN domain is present in several proteins related to the functions of Rap and Rab family GTPases. Accumulating evidence supports the hypothesis that RUN domain-containing proteins act as a component of vesicle traffic and might be responsible for an interaction with a filamentous network linked to actin cytoskeleton or microtubules. That is to say, on one hand, RUN domains associate with Rab or Rap family proteins, on the other hand, they also might interact with motor proteins such as kinesin or myosin via intervention molecules. In this review, we summarize the background and current status of RUN domain research with an emphasis on the interaction between RUN domain and motor proteins with respect to the vesicle traffic on filamentous network. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved., 2011年06月, 585, 12, 1707, 1710, 10.1016/j.febslet.2011.05.011
• 査読あり, 英語, Int J appl Biol pharm Technol, Ethanol extract of Rosemary repressed PTEN expression in K562 culture cells., 松田覚, 2011年, 2, 316-322
• 査読あり, 英語, J amino acids, Dicer functions in aquatic species., 松田覚, 2011年, 2011, 782187
• 査読あり, 日本語, 日本家政学会誌, 奈良近郊で販売された野菜などに含まれる硝酸態窒素量測定および簡便で効果的な除去法の検討, 松田覚; 井関詩緒他, 2010年12月, 61, 813-817
• 査読あり, 英語, INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES, Rab5(Q79L) interacts with the carboxyl terminus of RUFY3, Hitomi Yoshida; Naoko Okumura; Yasuko Kitagishi; Naoki Shirafuji; Satoru Matsuda, 2010年, 6, 2, 187, 189
• 査読あり, 英語, Int J Curr Res, Ubiquitin and proteasomes are involved in the degradation of cytosolic Doppel protein., 松田覚, 2010年, 5, 38-40
• 査読あり, 英語, ANNALS OF ONCOLOGY, Insulin receptor substrate protein 53 (IRSp53) as a binding partner of antimetastasis molecule NESH, a member of Abelson interactor protein family, S. Matsuda; S. Yokozaki; H. Yoshida; Y. Kitagishi; N. Shirafuji; N. Okumura, 2008年07月, 19, 7, 1356, U2, 10.1093/annonc/mdn293
• 査読あり, 英語, MOLECULAR ONCOLOGY, NESH protein expression switches to the adverse effect of imatinib mesylate, Satoru Matsuda; Yasukatu Ichigotani; Naoko Okumura; Hitomi Yoshida; Yuka Kajiya; Yasuko Kitagishi; Naoki Shirafuji, 2008年06月, 2, 1, 16, 19, 10.1016/j.molonc.2008.03.003
• 査読あり, 英語, FEBS LETTERS, NESH (Abi-3) is pre-sent in the Abi/WAVE complex but does not promote c-Abl-mediated phosphorylation, Noriko Hirao; Seiichi Sato; Tetsuya Gotoh; Masahiro Maruoka; Jun Suzuki; Satoru Matsuda; Tornoyuki Shishido; Katsuko Tani, Abl interactor (Abi) was identified as an Abl tyrosine kinase-binding protein and subsequently shown to be a component of the macromolecular Abi/WAVE complex, which is a key regulator of Rae-dependent actin polymerization. Previous studies showed that Abi-1 promotes c-Ab1-mediated phosphorylation of Mammalian Enabled (Mena) and WAVE2. In addition to Abi-1, mammals possess Abi-2 and NESH (Abi-3). In this study, we compared the three Abi proteins in terms of the promotion of c-Abl-mediated phosphorylation and the formation of Abi/WAVE complex. Although Abi-2, like Abi-1, promoted the c-Abl-mediated phosphorylation of Mena and WAVE2, NESH (Abi-3) had no such effect. This difference was likely due to their binding abilities as to c-Abl. Immunoprecipitation revealed that NESH (Abi-3) is present in the Abi/WAVE complex. Our results suggest that NESH (Abi-3), like Abi-1 and Abi-2, is a component of the Abi/WAVE complex, but likely plays a different role in the regulation of c-Abl. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved., 2006年11月, 580, 27, 6464, 6470, 研究論文（学術雑誌）, 10.1016/j.febslet.2006.10.065
• 査読あり, 英語, GENES TO CELLS, Interaction of anti-proliferative protein Tob with poly(A)-binding protein and inducible poly(A)-binding protein: implication of Tob in translational control, K Okochi; T Suzuki; J Inoue; S Matsuda; T Yamamoto, Tob is a member of an emerging family of anti-proliferative proteins that suppress cell growth when over-expressed. tob mRNA is highly expressed in anergic T cells and over-expression of Tob suppresses transcription of interleukin-2 (IL-2) through its interaction with Smads. Here, we identified two types of cDNA clones coding for poly(A)-binding protein (PABP) and inducible PABP (iPABP) by screening an expression cDNA library with the GST-Tob probe. Co-immunoprecipitation and GST-pull down experiments showed that Tob associated with the carboxyl-terminal region of iPABP. We then found that iPABP, like PABP, was involved in regulation of translation: iPABP enhanced translation of IL-2 mRNA in vitro. The enhanced translation of IL-2 mRNA required the 3'UTR and poly(A) sequences. Tob abrogated the enhancement of translation through its interaction with carboxyl-terminal region of iPABP in vitro. Consistently, over-expression of Tob in NIH3T3 cells, in which exogenous iPABP was stably expressed, resulted in suppression of IL-2 production from the simultaneously transfected IL-2 expression plasmid. Finally, Tob, whose expression was induced by anergic stimulation, was co-immunoprecipitated with iPABP in human T cells. These findings suggest that Tob is involved in the translational suppression of IL-2 mRNA in anergic T cells through its interaction with iPABP., 2005年02月, 10, 2, 151, 163, 研究論文（学術雑誌）, 10.1111/j.1365-2443.2005.00826.x
• 査読あり, 英語, Applied Biochemistry and Biotechnology - Part B Molecular Biotechnology, Intercept-PCR, an improvement for elevating performance to find a new member of a certain gene family, S. Matsuda; Y. Ichigotani; T. Okuda; K. Miyazaki; T. Yamamoto; Y. Nimura; T. Irimura; S. Nakatsugawa; M. Hamaguchi, We have established a method by which the performance of reverse transcriptase coupled polymerase chain reaction (RT-PCR) for seeking a new gene is improved. The actual procedure is quite easy: it is only to add several specific oligonucleotides into the reaction mixture of the usual RT-PCR. To verify the effectiveness of this method is also easy: it is only to detect the PCR products in the preliminary experiment. The finding in the present study provides valuable information for gene cloning tactics., 2000年, 16, 1, 1, 4, 研究論文（学術雑誌）
• 査読あり, 英語, International journal of preventive medicine, Prevention in Daily Life against Progression of COVID-19., Murakami M; Ikeda Y; Tsuji A; Matsuda S, 2020年07月, 11, 99, 99, 研究論文（学術雑誌）, 国際誌, 10.4103/ijpvm.IJPVM_219_20
• 査読あり, 英語, Biomedical Reports, Role of tumor suppressor molecules in genomic perturbations and damaged DNA repair involved in the pathogenesis of cancer and neurodegeneration (Review), Satoru Matsuda; Mutsumi Murakami; Yuka Ikeda; Yukie Nakagawa; Ai Tsuji; Yasuko χ Yasuko kitagishi, Genomic perturbations due to inaccurate DNA replication, including inappropriate chromosomal segregation often underlie the development of cancer and neurodegenerative diseases. The incidence of these two diseases increases with age and exhibits an inverse association. Therefore, elderly subjects with cancer exhibit a reduced risk of a neurodegenerative disease, and vice versa. Both of these diseases are associated with aging and share several risk factors. Cells have multiple mechanisms to repair DNA damage and inaccurate replication. Previous studies have demonstrated that tumor suppressor proteins serve a critical role in the DNA damage response, which may result in genomic instability and thus induction of cellular apoptosis. Tumor suppressor genes, such as phosphatase and tensin homologue deleted on chromosome 10 (PTEN), breast cancer susceptibility gene 1 (BRCA1) and TP53 reduce genomic susceptibility to cancer by repairing the damaged DNA. In addition, these genes work cooperatively to ensure the inhibition of the development of several types of cancer. PTEN, BRCA1 and TP53 have been recognized as the most frequently deleted and/or mutated genes in various types of human cancer. Recently, tumor suppressor genes have also been shown to be involved in the development of neurodegenerative diseases. The present review summarizes the recent findings of the functions of these tumor suppressors that are associated with genomic stability, and are involved in carcinogenic and neurodegenerative cell signaling. A summary is presented regarding the interactions of these tumor suppressors with their partners which results in transduction of downstream signals. The implications of these functions for cancer and neurodegenerative disease-associated biology are also highlighted., 2020年06月17日, 13, 3, 10, 10, 研究論文（学術雑誌）, 国際誌, 10.3892/br.2020.1317
• 査読あり, 英語, Biomedical Reports, Special bioactive compounds and functional foods may exhibit neuroprotective effects in patients with dementia (Review), Mutsumi Murakami; Yuka Ikeda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Dementia is a failure of cognitive ability characterized by severe neurodegeneration in select neural systems, and Alzheimer's disease (AD) is the most common type of neurodegenerative disease. Although numerous studies have provided insights into the pathogenesis of AD, the underlying signaling and molecular pathways mediating the progressive decline of cognitive function remain poorly understood. Recent progress in molecular biology has provided an improved understanding of the importance of molecular pathogenesis of AD, and has proposed an association between DNA repair mechanisms and AD. In particular, the fundamental roles of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and breast cancer gene 1 (BRCA1) tumor suppressors have been shown to regulate the pathogenesis of neurodegeneration. Consequently, onset of neurodegenerative diseases may be deferred with the use of dietary neuroprotective agents which alter the signaling mediated by the aforementioned tumor suppressors. In a healthy neuron, homeostasis of key intracellular molecules is of great importance, and preventing neuronal apoptosis is one of the primary goals of treatments designed for dementia-associated diseases. In the present review, progress into the understanding of dietary regulation for preventing or limiting development of dementia is discussed with a focus on the modulatory roles of PTEN and BRCA1 signaling., 2020年06月02日, 13, 2, 1, 1, 研究論文（学術雑誌）, 国際誌, 10.3892/br.2020.1310
• 査読あり, 英語, Biomedical Reports, Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review), Yuka Ikeda; Mutsumi Murakami; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Fatty liver disease (FLD) is characterized by accumulation of excess fat in the liver. The underlying molecular mechanism associated with the progression of the disease has been in elusive. Hepatocellular demise due to increased oxidative stress resulting in an inflammatory response may be a key feature in FLD. Recent advances in molecular biology have led to an improved understanding of the molecular pathogenesis, suggesting a critical association between the PI3K/AKT/PTEN signaling pathway and FLD. In particular, PTEN has been associated with regulating the pathogenesis of hepatocyte degeneration. Given the function of mitochondria in reactive oxygen species (ROS) generation and the initiation of oxidative stress, the mitochondrial antioxidant network is of interest. It is vital to balance the activity of intracellular key molecules to maintain a healthy liver. Consequently, onset of FLD may be delayed using dietary protective agents that alter PTEN signaling and reduce ROS levels. The advancement of research on dietary regulation with a focus on modulatory roles in ROS generation and PTEN associated signaling is summarized in the current study, supporting further preventive and therapeutic exploration., 2020年04月22日, 12, 6, 295, 302, 研究論文（学術雑誌）, 国際誌, 10.3892/br.2020.1299
• 査読あり, その他, Biomedical Journal of Scientific & Technical Research, Is Lockdown Effective Against Fatality of COVID-19?, Satoru Matsuda, 2020年07月17日, 28, 5, 研究論文（学術雑誌）, 10.26717/bjstr.2020.28.004729
• 査読あり, その他, Journal of Advances in Medicine and Medical Research, Save Children from Mortal Shock of COVID-19, Satoru Matsuda; Yuka Ikeda; Mutsumi Murakami; Ai Tsuji, Letter to the Editor, 2020年06月05日, 23, 25, 研究論文（学術雑誌）, 10.9734/jammr/2020/v32i830462
• 査読あり, その他, Clinical Obstetrics, Gynecology and Reproductive Medicine, COVID-19, an infertility risk?, Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Satoru Matsuda, 2020年, 6, 3, 研究論文（学術雑誌）, 10.15761/cogrm.1000291
• 査読あり, その他, AIMS Molecular Science, Cigarette smoke may be an exacerbation factor in nonalcoholic fatty liver disease via modulation of the PI3K/AKT pathway, Mayuko Ichimura; Akari Minami; Noriko Nakano; Yasuko Kitagishi; Toshiyuki Murai; Satoru Matsuda, 2015年, 2, 4, 427, 439, 研究論文（学術雑誌）, 10.3934/molsci.2015.4.427
• 査読あり, その他, Oncogene, A role for SHPS-1/SIRPα1 in IL-1β- and TNFα-dependent signaling, Ali Reja Mohammad Ruhul Amin; Kazuya Machida; Kumi Oshima; Myat Lin Oo; Aye Aye Thant; Takeshi Senga; Satoru Matsuda; Anwarul Azim Akhand; Akito Maeda; Tomohiro Kurosaki; Michinari Hamaguchi, 2002年12月, 21, 57, 8871, 8878, 研究論文（学術雑誌）, 10.1038/sj.onc.1206018
• 査読あり, その他, Oncol Rep ., Expression of p73 gene, cell proliferation and apoptosis in breast cancer: Immunohistochemical and clinicopathological study, Tatsuyoshi Yamamoto; Koji Oda; Tomoyuki Kubota; Kou Miyazaki; Yasushi Takenouti; Yuji Nimura; Michinari Hamaguchi; Satoru Matsuda, 2002年08月, 9, 4, 729, 735
• 査読あり, その他, Cancer Res., SHPS-1: a budding molecule against cancer dissemination., Oshima K; Machida K; Ichigotani Y; Nimura Y; Shirafuji N; Hamaguchi M; Matsuda S, 2002年07月, 62, 14, 3929, 3933
• 査読あり, その他, Cancer Res., Hyaluronan-CD44s signaling regulates matrix metalloproteinase-2 secretion in a human lung carcinoma cell line QG90, Zhang Y; Thant AA; Machida K; Ichigotani Y; Naito Y; Hiraiwa Y; Senga T; Sohara Y; Matsuda S; Hamaguchi M, 2002年07月, 62, 14, 3962, 3965
• 査読あり, その他, In search of a function for the E3B1/Abi2/Argbp1/NESH family, Ichigotani Y; Fujii K; Hamaguchi M; Matsuda S, 2002年06月, 9, 6, 591, 595
• 査読あり, その他, FEBS Letters, SHPS-1, a multifunctional transmembrane glycoprotein, Kumi Oshima; A.R.M Ruhul Amin; Atsushi Suzuki; Michinari Hamaguchi; Satoru Matsuda, 2002年05月22日, 519, 1-3, 1, 7, 研究論文（学術雑誌）, 10.1016/s0014-5793(02)02703-5
• 査読あり, その他, Cancer Res., Forced expression of NESH suppresses motility and metastatic dissemination of malignant cells, Ichigotani Y; Yokozaki S; Fukuda Y; Hamaguchi M; Matsuda S, 2002年04月, 62, 8, 2215, 2219
• 査読あり, その他, Biochemical and Biophysical Research Communications, A Role for Focal Adhesion Kinase in Hyluronan-Dependent MMP-2 Secretion in a Human Small-Cell Lung Carcinoma Cell Line, QG90, Yanying Zhang; Aye Aye Thant; Yukiko Hiraiwa; Yuko Naito; Thet Thet Sein; Yasuyoshi Sohara; Satoru Matsuda; Michinari Hamaguchi, 2002年01月, 290, 3, 1123, 1127, 研究論文（学術雑誌）, 10.1006/bbrc.2001.6321
• 査読あり, その他, Histol Histopathol., STAT and SMAD signaling in cancer., Iwamoto T; Oshima K; Seng T; Feng X; Oo ML; Hamaguchi M; Matsuda S, 2002年, 17, 3, 887, 895
• 査読あり, その他, Oncogene, Suppression of cell spreading by v-Crk requires Ras-MEK-MAP kinase signaling, Yuzhen Liu; Yukiko Hiraiwa; Enbo Liu; Hisashi Kurata; Aye Aye Thant; Satoru Matsuda; Michinari Hamaguchi, 2001年09月, 20, 41, 5908, 5912, 研究論文（学術雑誌）, 10.1038/sj.onc.1204738
• 査読あり, その他, International Journal of Oncology, p73 is highly expressed in myoepithelial cells and in carcinomas with metaplasia, Tatsuyoshi Yamamoto; Koji Oda; Kou Miyazaki; Yasukatu Ichigotani; Yasushi Takenouchi; Tomotaka Kamei; Naoki Shirafuji; Yuji Nimura; Michinari Hamaguchi; Satoru Matsuda, 2001年08月01日, 研究論文（学術雑誌）, 10.3892/ijo.19.2.271
• 査読あり, 英語, Journal of human genetics, Springer-Verlag Tokyo, Cloning and sequencing of a novel human gene that encodes a putative target protein of Nesh-SH3, Matsuda Satoru; Iriyama Chisako; Yokozaki Shouichi; ICHIGOTANI Yasukatu; SHIRAFUJI Naoki; YAMAKI Kenichi; HAYAKAWA Tetsuo; HAMAGUCHI Michinari, 2001年08月, 46, 8, 483, 486, 研究論文（学術雑誌）, 10.1007/s100380170049
• 査読あり, その他, Molecular Biology of the Cell, Hyaluronan Activates Cell Motility of v-Src-transformed Cells via Ras-Mitogen–activated Protein Kinase and Phosphoinositide 3-Kinase-Akt in a Tumor-specific Manner, Yasuyoshi Sohara; Naoki Ishiguro; Kazuya Machida; Hisashi Kurata; Aye Aye Thant; Takeshi Senga; Satoru Matsuda; Koji Kimata; Hisashi Iwata; Michinari Hamaguchi, We investigated the production of hyaluronan (HA) and its effect on cell motility in cells expressing the v-src mutants. Transformation of 3Y1 by v-src virtually activated HA secretion, whereas G2A v-src, a nonmyristoylated form of v-src defective in cell transformation, had no effect. In cells expressing the temperature-sensitive mutant of v-Src, HA secretion was temperature dependent. In addition, HA as small as 1 nM, on the other side, activated cell motility in a tumor-specific manner. HA treatment strongly activated the motility of v-Src–transformed 3Y1, whereas it showed no effect on 3Y1- and 3Y1-expressing G2A v-src. HA-dependent cell locomotion was strongly blocked by either expression of dominant-negative Ras or treatment with a Ras farnesyltransferase inhibitor. Similarly, both the MEK1 inhibitor and the kinase inhibitor clearly inhibited HA-dependent cell locomotion. In contrast, cells transformed with an active MEK1 did not respond to the HA. Finally, an anti-CD44–neutralizing antibody could block the activation of cell motility by HA as well as the HA-dependent phosphorylation of mitogen-activated protein kinase and Akt. Taken together, these results suggest that simultaneous activation of the Ras-mitogen-activated protein kinase pathway and the phosphoinositide 3-kinase pathway by the HA-CD44 interaction is required for the activation of HA-dependent cell locomotion in v-Src–transformed cells., 2001年06月, 12, 6, 1859, 1868, 研究論文（学術雑誌）, 10.1091/mbc.12.6.1859
• 査読あり, その他, Journal of Human Genetics, Cloning and sequencing of a novel human gene which encodes a putative hydroxylase, C. Iriyama; S. Matsuda; R. Katsumata; M. Hamaguchi, 2001年04月, 46, 5, 289, 292, 研究論文（学術雑誌）, 10.1007/s100380170081
• 査読あり, 英語, Genes to Cells, A serine/threonine kinase p90rsk1 phosphorylates the anti-proliferative protein Tob, Toru Suzuki; Satoru Matsuda; Junko K. Tsuzuku; Yutaka Yoshida; Tadashi Yamamoto, BACKGROUND: tob is a member of a gene family with anti-proliferative function. Over-expression of Tob in NIH3T3 cells results in the suppression of cell proliferation. The growth suppression is hampered by the presence of activated ErbB2 kinase. The molecular mechanisms by which Tob suppresses cell growth and by which ErbB2 abrogates Tob function remain to be elucidated. RESULTS: We show that Tob is phosphorylated on serines and threonines, but not tyrosines, by a kinase(s) that associates with Tob in the lysates of various cells, including ErbB2-over-expressed cells. We also show that a 95 kDa kinase associates with Tob in vitro. The autophosphorylation activity of this kinase co-chromatographes with Tob-phosphorylating activity, suggesting that the 95 kDa kinase phosphorylates Tob. Among the known kinases with molecular mass around 95 kDa, p90rsk1 associates with Tob in vitro and in vivo, and phosphorylates Tob at least in vitro. Therefore, it is likely that p90rsk1 represents the 95 kDa kinase and is involved in the regulation of Tob function through phosphorylation. CONCLUSION: p90rsk1 associates with and phosphorylates Tob. Because p90rsk1 is activated downstream of receptor tyrosine kinases, we propose that Tob function is at least in part under the control of growth factor-stimulated tyrosine kinases through its phosphorylation by p90rsk1., 2001年02月, 6, 2, 131, 138, 研究論文（学術雑誌）, 国際誌, 10.1046/j.1365-2443.2001.00406.x
• 査読あり, その他, Oncogene, A role for FAK in the Concanavalin A-dependent secretion of matrix metalloproteinase-2 and -9, Thet Thet Sein; Aye Aye Thant; Yukiko Hiraiwa; ARM Ruhul Amin; Yasuyoshi Sohara; Yuzhen Liu; Satoru Matsuda; Tadashi Yamamoto; Michinari Hamaguchi, 2000年11月, 19, 48, 5539, 5542, 研究論文（学術雑誌）, 10.1038/sj.onc.1203932
• 査読あり, 英語, Journal of human genetics, Springer-Verlag Tokyo, Molecular cloning of a novel human gene (SIRP-B2) which encodes a new member of the SIRP/SHPS-1 protein family, Ichigotani Yasukatu; Matsuda Satoru; Machida Kazuya; OSHIMA Kumi; IWAMOTO Takashi; YAMAKI Kenichi; HAYAKAWA Tetsuo; HAMAGUCHI Michinari, 2000年11月, 45, 6, 378, 382, 研究論文（学術雑誌）, 10.1007/s100380070013
• 査読あり, その他, Journal of Biological Chemistry, Constitutive Tyrosine Phosphorylation of ErbB-2 via Jak2 by Autocrine Secretion of Prolactin in Human Breast Cancer, Toshimasa Yamauchi; Naoko Yamauchi; Kohjiro Ueki; Takuya Sugiyama; Hironori Waki; Hiroshi Miki; Kazuyuki Tobe; Satoru Matsuda; Toshio Tsushima; Tadashi Yamamoto; Toshiro Fujita; Yuji Taketani; Masashi Fukayama; Satoshi Kimura; Yoshio Yazaki; Ryozo Nagai; Takashi Kadowaki, 2000年10月, 275, 43, 33937, 33944, 研究論文（学術雑誌）, 10.1074/jbc.m000743200
• 査読あり, その他, Oncogene, The JAK-inhibitor, JAB/SOCS-1 selectively inhibits cytokine-induced, but not v-Src induced JAK–STAT activation, Takashi Iwamoto; Takeshi Senga; Yuko Naito; Satoru Matsuda; Yozo Miyake; Akihiko Yoshimura; Michinari Hamaguchi, 2000年09月, 19, 41, 4795, 4801, 研究論文（学術雑誌）, 10.1038/sj.onc.1203829
• 査読あり, その他, International Journal of Oncology, C-Cbl protein in human cancer tissues is frequently tyrosine phosphorylated in a tumor-specific manner., T Kamei; K Machida; Y Nimura; T Senga; I Yamada; S Yoshii; S Matsuda; M Hamaguchi, 2000年08月01日, 研究論文（学術雑誌）, 10.3892/ijo.17.2.335
• 査読あり, その他, Cancer Res., The Ras-mitogen-activated protein kinase pathway is critical for the activation of matrix metalloproteinase secretion and the invasiveness in v-crk-transformed 3Y1., Liu E; Thant AA; Kikkawa F; Kurata H; Tanaka S; Nawa A; Mizutani S; Matsuda S; Hanafusa H; Hamaguchi M, 2000年05月, 60, 9, 2361, 2364
• 査読あり, その他, Oncogene, Clustered cysteine residues in the kinase domain of v-Src: critical role for protein stability, cell transformation and sensitivity to herbimycin A, Takeshi Senga; Kou Miyazaki; Kazuya Machida; Hiroyuki Iwata; Satoru Matsuda; Izumi Nakashima; Michinari Hamaguchi, 2000年01月, 19, 2, 273, 279, 研究論文（学術雑誌）, 10.1038/sj.onc.1203296
• 査読あり, その他, Oncogene, Ras pathway is required for the activation of MMP-2 secretion and for the invasion of src-transformed 3Y1, Aye Aye Thant; Thet Thet Sein; Enbo Liu; Kazuya Machida; Fumitaka Kikkawa; Teruhiko Koike; Motoharu Seiki; Satoru Matsuda; Michinari Hamaguchi, 1999年11月, 18, 47, 6555, 6563, 研究論文（学術雑誌）, 10.1038/sj.onc.1203049
• 査読あり, その他, Biochemical and Biophysical Research Communications, Critical Amino Acid Substitutions in the Src SH3 Domain That Convert c-Src to Be Oncogenic, Kou Miyazaki; Takeshi Senga; Satoru Matsuda; Miho Tanaka; Kazuya Machida; Yasushi Takenouchi; Yuji Nimura; Michinari Hamaguchi, 1999年10月, 263, 3, 759, 764, 研究論文（学術雑誌）, 10.1006/bbrc.1999.1464
• 査読あり, その他, Biochemical and Biophysical Research Communications, Molecular Cloning of Macrophin, a Human Homologue of Drosophila Kakapo with a Close Structural Similarity to Plectin and Dystrophin, Takahito Okuda; Satoru Matsuda; Shigekazu Nakatsugawa; Yasukatu Ichigotani; Naoko Iwahashi; Masahide Takahashi; Takeo Ishigaki; Michinari Hamaguchi, 1999年10月, 264, 2, 568, 574, 研究論文（学術雑誌）, 10.1006/bbrc.1999.1538
• 査読あり, その他, Oncogene, ANA, a novel member of Tob/BTG1 family, is expressed in the ventricular zone of the developing central nervous system, Yutaka Yoshida; Satoru Matsuda; Naoko Ikematsu; Junko Kawamura-Tsuzuku; Johji Inazawa; Hisashi Umemori; Tadashi Yamamoto, 1998年05月, 16, 20, 2687, 2693, 研究論文（学術雑誌）, 10.1038/sj.onc.1201805
• 査読あり, その他, International Journal of Oncology, Suppression of cell growth by ectopic expression of N-cadherin., X Wang; A A Thant; K Machida; Y Hiraiwa; H Iwata; S Matsuda; M Hamaguchi, 1998年05月01日, 研究論文（学術雑誌）, 10.3892/ijo.12.5.1097
• 査読あり, その他, Genes, Chromosomes and Cancer, Homozygous deletion and frequent allelic loss of the 21q11.1-q21.1 region including theANA gene in human lung carcinoma, Takashi Kohno; Masashi Kawanishi; Satoru Matsuda; Hitoshi Ichikawa; Minoru Takada; Misao Ohki; Tadashi Yamamoto; Jun Yokota, 1998年03月, 21, 3, 236, 243, 研究論文（学術雑誌）, 10.1002/(sici)1098-2264(199803)21:3<236::aid-gcc8>3.0.co;2-0
• 査読あり, その他, Advances in Experimental Medicine and Biology, Inhibition of Human Pancreatic Cancer Growth by the Adenovirus-Mediated Introduction of a Novel Growth Suppressing Gene, tob, In Vitro, Hironobu Yanagie; H. Sumimoto; Y. Nonaka; S. Matsuda; I. Hirose; S. Hanada; H. Sugiyama; S. Mikamo; Y. Takeda; I. Yoshizaki; K. Nakazawa; K. Tani; T. Yamamoto; S. Asano; M. Eriguchi; T. Muto, 1998年, 91, 96, 論文集(書籍)内論文, 10.1007/978-1-4615-5357-1_15
• 査読あり, その他, J. Biol. Chem., Molecular cloning and characterization of a novel cytoplasmic protein-tyrosine phosphatase that is specifically expressed in spermatocytes, OHSUGI M., 1997年12月, 272, 52, 33092, 33099, 研究論文（学術雑誌）, 10.1074/jbc.272.52.33092
• 査読あり, その他, Mitochondrial antisense RNA for cytochrome C oxidase (MARCO) can induce morphologic changes and cell death in human hematopoietic cell lines, Shirafuji N; Takahashi S; Matsuda S; Asano S, 1997年12月, 90, 11, 4567, 4577
• 査読あり, その他, Gene, A novel zinc finger protein, Finb, is a transcriptional activator and localized in nuclear bodies, Akiko Fujimoto-Nishiyama; Shunsuke Ishii; Satoru Matsuda; Jun-ichiro Inoue; Tadashi Yamamoto, 1997年08月, 195, 2, 267, 275, 研究論文（学術雑誌）, 10.1016/s0378-1119(97)00172-8
• 査読あり, その他, Gene, Cloning and characterization of the mouse tob gene, Yutaka Yoshida; Satoru Matsuda; Tadashi Yamamoto, 1997年05月, 191, 1, 109, 113, 研究論文（学術雑誌）, 10.1016/s0378-1119(97)00049-8
• 査読あり, その他, FEBS Letters, Molecular cloning and characterization of Byp, a murine receptor-type tyrosine phosphatase similar to human DEP-1, Satomi Kuramochi; Satoru Matsuda; Yoichi Matsuda; Toshiyuki Saitoh; Miho Ohsugi; Tadashi Yamamoto, 1996年01月02日, 378, 1, 7, 14, 研究論文（学術雑誌）, 10.1016/0014-5793(95)01415-2
• 査読あり, その他, Int.Immunol., Characterization of p56^^-mediated signal transduction on T cell activation., FUSAKI N., 1994年, 6, 8, 1245, 1255, 研究論文（学術雑誌）, 10.1093/intimm/6.8.1245
• 査読あり, その他, Proceedings of the National Academy of Sciences, 17 beta-estradiol mimics ligand activity of the c-erbB2 protooncogene product., S. Matsuda; Y. Kadowaki; M. Ichino; T. Akiyama; K. Toyoshima; T. Yamamoto, 1993年11月15日, 90, 22, 10803, 10807, 研究論文（学術雑誌）, 10.1073/pnas.90.22.10803
• 査読あり, その他, Japanese Journal of Cancer Research, Detection of the Ligand Activity of thec-erbB-2Protein in Calf Serum, RuJiao Shan; Satoru Matsuda; Motohide Ichino; Tadashi Yamamoto, 1992年01月, 83, 1, 15, 19, 研究論文（学術雑誌）, 10.1111/j.1349-7006.1992.tb02345.x
• 査読あり, その他, Biochemical and Biophysical Research Communications, Active c-erbB-2 induces short-term growth of FDC-P2 cells after IL-3 depletion, Budsaba Wongsasant; Satoru Matsuda; Tadashi Yamamoto, 1991年12月, 181, 3, 981, 988, 研究論文（学術雑誌）, 10.1016/0006-291x(91)92033-g
• 査読あり, その他, Granulocyte colony-stimulating factor stimulates human mature neutrophilic granulocytes to produce interferon-alpha, Shirafuji N; Matsuda S; Ogura H; Tani K; Kodo H; Ozawa K; Nagata S; Asano S; Takaku F, 1990年01月, 75, 1, 17, 19
• 査読あり, その他, Human granulocyte colony-stimulating factor specifically binds to murine myeloblastic NFS-60 cells and activates their guanosine triphosphate binding proteins/adenylate cyclase system, Matsuda S; Shirafuji N; Asano S, 1989年11月, 74, 7, 2343, 2348
• 査読あり, その他, Journal of Biological Chemistry, A new bioassay for human granulocyte colony-stimulating factor (hG-CSF) using murine myeloblastic NFS-60 cells as targets and estimation of its levels in sera from normal healthy persons and patients with infectious and hematological disorders., Shirafuji N; Asano S; Matsuda S; Watari K; Takaku F; Nagata S, 1989年02月, 17, 2, 116, 119, 研究論文（学術雑誌）, 10.1074/jbc.272.28.17668
• 査読あり, その他, Leukemia Research, Production of granulocyte colony-stimulating factor by acute myelomonocytic leukemia cells, Naoki Shirafuji; Shigetaka Asano; Koji Kozai; Satoshi Takahashi; Satoru Matsuda; Fumimaro Takaku; Shigekazu Nagata, 1988年01月, 12, 9, 745, 750, 研究論文（学術雑誌）, 10.1016/0145-2126(88)90007-0
• 査読あり, 英語, Livers, Metabolic Associated Fatty Liver Disease as a Risk Factor for the Development of Central Nervous System Disorders, Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Tomoko Asai; Ai Tsuji; Satoru Matsuda, MAFLD/NAFLD is the most ordinary liver disease categorized by hepatic steatosis with the increase of surplus fat in the liver and metabolic liver dysfunction, which is associated with bigger mortality and a high medical burden. An association between MAFLD/NAFLD and central nervous system disorders including psychological disorders has been demonstrated. Additionally, MAFLD/NAFLD has been correlated with various types of neurodegenerative disorders such as amyotrophic lateral sclerosis or Parkinson’s disease. Contrasted to healthy controls, patients with MAFLD/NAFLD have a greater prevalence risk of extrahepatic complications within multiple organs. Dietary interventions have emerged as effective strategies for MAFLD/NAFLD. The PI3K/AKT/mTOR signaling pathway involved in the regulation of Th17/Treg balance might promote the pathogenesis of several diseases including MAFLD/NAFLD. As extrahepatic complications may happen across various organs including CNS, cooperative care with individual experts is also necessary for managing patients with MAFLD/NAFLD., 2023年01月05日, 3, 1, 21, 32, 研究論文（学術雑誌）, 10.3390/livers3010002
• 査読あり, 英語, Exploration of Targeted Anti-tumor Therapy, Encouraging probiotics for the prevention and treatment of immune-related adverse events in novel immunotherapies against malignant glioma, Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Satoru Matsuda, Among the malignant tumors in the central nervous system (CNS), glioma is the most challenging tumor to the public society, which accounts for the majority of intracranial malignant tumors with impaired brain function. In general, conventional therapies are still unable to provide an effective cure. However, novel immunotherapies have changed the treatment scene giving patients a greater potential to attain long term survival, improved quality of life. Having shown favorable results in solid tumors, those therapies are now at a cancer research hotspot, which could even shrink the growth of glioma cells without causing severe complications. However, it is important to recognize that the therapy may be occasionally associated with noteworthy adverse action called immune-related adverse events (IRAEs) which have emerged as a potential limitation of the therapy. Multiple classes of mediators have been developed to enhance the ability of immune system to target malignant tumors including glioma but may also be associated with the IRAEs. In addition, it is probable that it would take long time after the therapy to exhibit severe immune-related disorders. Gut microbiota could play an integral role in optimal immune development and/or appropriate function for the cancer therapy, which is a vital component of the multidirectional communication between immune system, brain, and gut, also known as gut-brain-immune axis. Here, we show the potential effects of the gut-brain-immune axis based on an “engram theory” for the innovative treatment of IRAEs., 2022年12月27日, 3, 6, 817, 827, 研究論文（学術雑誌）, 国際誌, 10.37349/etat.2022.00114
• 査読あり, 英語, Biomolecules, Encouraging Tactics with Genetically Modified Probiotics to Improve Immunity for the Prevention of Immune-Related Diseases including Cardio-Metabolic Disorders, Tomoko Asai; Sayuri Yoshikawa; Yuka Ikeda; Kurumi Taniguchi; Haruka Sawamura; Ai Tsuji; Satoru Matsuda, The PI3K/AKT/mTOR signaling pathway may play crucial roles in the pathogenesis of obesity and diabetes mellitus, as well as metabolic syndromes, which could also be risk factors for cardio-metabolic disorders. Consistently, it has been shown that beneficial effects may be convoyed by the modulation of the PI3K/AKT/mTOR pathway against the development of these diseases. Importantly, the PI3K/AKT/mTOR signaling pathway can be modulated by probiotics. Probiotics have a variety of beneficial properties, with the potential of treating specific diseases such as immune-related diseases, which are valuable to human health. In addition, an increasing body of work in the literature emphasized the contribution of genetically modified probiotics. There now seems to be a turning point in the research of probiotics. A better understanding of the interactions between microbiota, lifestyle, and host factors such as genetics and/or epigenetics might lead to a novel therapeutic approach with probiotics for these diseases. This study might provide a theoretical reference for the development of genetically modified probiotics in health products and/or in functional foods for the treatment of cardio-metabolic disorders., 2022年12月21日, 13, 1, 10, 10, 研究論文（学術雑誌）, 国際誌, 10.3390/biom13010010
• 査読あり, 英語, Diseases, Potential Diets to Improve Mitochondrial Activity in Amyotrophic Lateral Sclerosis, Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Satoru Matsuda, Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease, the pathogenesis of which is based on alternations in the mitochondria of motor neurons, causing their progressive death. A growing body of evidence shows that more efficient mitophagy could prevent and/or treat this disorder by suppressing mitochondrial dysfunction-induced oxidative stress and inflammation. Mitophagy has been considered one of the main mechanisms responsible for mitochondrial quality control. Since ALS is characterized by enormous oxidative stress, several edible phytochemicals that can activate mitophagy to remove damaged mitochondria could be considered a promising option to treat ALS by providing neuroprotection. Therefore, it is of great significance to explore the mechanisms of mitophagy in ALS and to understand the effects and/or molecular mechanisms of phytochemical action, which could translate into a treatment for neurodegenerative diseases, including ALS., 2022年12月01日, 10, 4, 117, 117, 研究論文（学術雑誌）, 国際誌, 10.3390/diseases10040117
• 査読あり, 英語, Metabolites, A New Concept of Associations between Gut Microbiota, Immunity and Central Nervous System for the Innovative Treatment of Neurodegenerative Disorders, Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Satoru Matsuda, Nerve cell death accounts for various neurodegenerative disorders, in which altered immunity to the integrated central nervous system (CNS) might have destructive consequences. This undesirable immune response often affects the progressive neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, schizophrenia and/or amyotrophic lateral sclerosis (ALS). It has been shown that commensal gut microbiota could influence the brain and/or several machineries of immune function. In other words, neurodegenerative disorders may be connected to the gut–brain–immune correlational system. The engrams in the brain could retain the information of a certain inflammation in the body which might be involved in the pathogenesis of neurodegenerative disorders. Tactics involving the use of probiotics and/or fecal microbiota transplantation (FMT) are now evolving as the most promising and/or valuable for the modification of the gut–brain–immune axis. More deliberation of this concept and the roles of gut microbiota would lead to the development of stupendous treatments for the prevention of, and/or therapeutics for, various intractable diseases including several neurodegenerative disorders., 2022年11月01日, 12, 11, 1052, 1052, 研究論文（学術雑誌）, 国際誌, 10.3390/metabo12111052
• 査読あり, 英語, Exploration of Medicine, A budding concept with certain microbiota, anti-proliferative family proteins, and engram theory for the innovative treatment of colon cancer, Yuka Ikeda; Kurumi Taniguchi; Sayuri Yoshikawa; Haruka Sawamura; Ai Tsuji; Satoru Matsuda, Inflammatory bowel disease (IBD) is a multifactorial chronic disease. Patients with IBD have an increased risk of developing colorectal cancer which has become a major health concern. IBD might exert a role of engrams for making the condition of specific inflammation in the gut. Dysregulation of immune cells induced by the command of engrams might be crucial in the pathogenesis of damages in gut epithelium. The anti-proliferative (APRO) family of anti-proliferative proteins characterized by immediate early responsive gene-products that might be involved in the machinery of the carcinogenesis in IBD. Herein, it is suggested that some probiotics with specific bacteria could prevent the development and/or progression of the IBD related tumors. In addition, consideration regarding the application of studying APRO family proteins for the comprehension of IBD related tumors has been presented. It is hypothesized that overexpression of Tob1, a member of APRO family proteins, in the epithelium of IBD could suppress the function of adjacent cytotoxic immune cells possibly via the paracrine signaling., 2022年10月27日, 2, 3, 468, 478, 研究論文（学術雑誌）, 10.37349/emed.2022.00108
• 査読あり, 英語, Cancers, Presumed Roles of APRO Family Proteins in Cancer Invasiveness, Yuka Ikeda; Kurumi Taniguchi; Haruka Sawamura; Sayuri Yoshikawa; Ai Tsuji; Satoru Matsuda, The APRO family members may be involved in the regulation of cell growth, migration, and/or invasion. Although an APRO protein could suppress the invasiveness of several cancer cells, it has been reported that overexpression of the same APRO protein could also promote the invasiveness and/or metastasis of the same cancer cells. In general, the invasiveness of cancer cells might be associated with the function of matrix metalloproteinases (MMPs) as well as with the function of certain exosomes. However, it has been shown that exosomes involving particular APRO proteins, MMPs, and/or microRNA could contribute to the regulation of invasiveness. Here, we discuss contradictory reports on invasiveness in relation to APRO family proteins on the basis of understanding the function of MMPs and/or various exosomes. A better understanding of those mechanisms could be of use to bring about innovative strategies for cancer treatment., 2022年10月08日, 14, 19, 4931, 4931, 研究論文（学術雑誌）, 国際誌, 10.3390/cancers14194931
• 査読あり, 英語, World Journal of Gastroenterology, Promising role of D-amino acids in irritable bowel syndrome, Yuka Ikeda; Kurumi Taniguchi; Haruka Sawamura; Ai Tsuji; Satoru Matsuda, Irritable bowel syndrome (IBS) is an important health care concern. Alterations in the microbiota of the gut-brain axis may be linked to the pathophysiology of IBS. Some dietary intake could contribute to produce various metabolites including D-amino acids by the fermentation by the gut microbiota. D-amino acids are the enantiomeric counterparts of L-amino acids, in general, which could play key roles in cellular physiological processes against various oxidative stresses. Therefore, the presence of D-amino acids has been shown to be linked to the protection of several organs in the body. In particular, the gut microbiota could play significant roles in the stability of emotion via the action of D-amino acids. Here, we would like to shed light on the roles of D-amino acids, which could be used for the treatment of IBS., 2022年08月21日, 28, 31, 4471, 4474, 研究論文（学術雑誌）, 国際誌, 10.3748/wjg.v28.i31.4471
• 査読あり, 英語, Oxygen, Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury, Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Satoru Matsuda, Cisplatin-induced acute kidney injury (AKI) is the main factor restraining the clinical application of cisplatin. The AKI is associated with high mortality and morbidity, but no effective pharmacological treatment is available at present. As increased levels of reactive oxygen species (ROS) may promote the progression of the injury, the elimination of ROS has been considered as an effective method to prevent the cisplatin-induced AKI. In addition, it has been revealed that an inducer of autophagy could protect kidney cells in the autophagy dependent manner. Induction of autophagy could also modulate the production of ROS in cases of renal injury. Therefore, kidney-targeted antioxidants and/or autophagy are urgently required for the better treatment of AKI. Accumulating evidence has indicated the important roles of gut microbiota in the pathogenesis of AKI. In addition, there is a scientific basis for considering future clinical applications of probiotics and/or prebiotics to treat cisplatin-induced AKI. Thus, gut microbiota might be a promising therapeutic target via the alteration of autophagy for the cancer therapy-induced nephrotoxicity., 2022年08月05日, 2, 3, 317, 326, 研究論文（学術雑誌）, 10.3390/oxygen2030022
• 査読あり, 英語, Exploration of Neuroprotective Therapy, Gut microbiota could modulate the effects of neuro-immune responses and memory traces via the gut-brain-immune axis in schizophrenia, Haruka Sawamura; Kurumi Taniguchi; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Altered immunity may have destructive consequences for the integrated central nervous system. This immune response often affects progressive neurodegenerative diseases such as Parkinson’s disease and/or psychiatric disorders such as schizophrenia. In particular, schizophrenia pathogenesis may be mediated by multiple neuro-immune interaction pathways. Gut microbiota might affect the brain and/or immune function. Significant machineries of immunity are commonly affected by the commensal gut microbiota. Therefore, schizophrenia may be connected with the gut-immune system. In addition, the brain and immune systems cooperate on multiple levels. The brain could save several pieces of information about specific inflammation in a body. This immunological memory named “engrams”, also called memory traces, could restore the initial disease state, which may help to explain key features of schizophrenia. Based on this concept, therapeutic strategies for schizophrenia could be the modification of the gut microbiota. Probiotics and/or fecal microbiota transplantation are now emerging as the most promising treatments for the modification. More consideration of the roles of gut microbiota will conduct the further development of immune-based therapeutics for the prevention and/or treatments of psychiatric disorders., 2022年04月24日, 74, 86, 研究論文（学術雑誌）, 10.37349/ent.2022.00019
• 査読あり, 英語, World Journal of Diabetes, Efficacy of probiotics on the modulation of gut microbiota in the treatment of diabetic nephropathy, Nozomi Nagase; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Diabetic nephropathy (DN) is a major cause of end-stage renal disease, and therapeutic options for preventing its progression are insufficient. The number of patients with DN has been increasing in Asian countries because of westernization of dietary lifestyle, which may be associated with the following changes in gut microbiota. Alterations in the gut microbiota composition can lead to an imbalanced gastrointestinal environment that promotes abnormal production of metabolites and/or inflammatory status. Functional microenvironments of the gut could be changed in the different stages of DN. In particular, altered levels of short chain fatty acids, D-amino acids, and reactive oxygen species biosynthesis in the gut have been shown to be relevant to the pathogenesis of the DN. So far, evidence suggests that the gut microbiota may play a key role in determining networks in the development of DN. Interventions directing the gut microbiota deserve further investigation as a new protective therapy in DN. In this review, we discuss the potential roles of the gut microbiota and future perspectives in the protection and/or treatment of kidneys., 2022年03月15日, 13, 3, 150, 160, 研究論文（学術雑誌）, 国際誌, 10.4239/wjd.v13.i3.150
• 査読あり, 英語, Diseases, D-Amino Acids as a Biomarker in Schizophrenia, Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, D-amino acids may play key roles for specific physiological functions in different organs including the brain. Importantly, D-amino acids have been detected in several neurological disorders such as schizophrenia, amyotrophic lateral sclerosis, and age-related disorders, reflecting the disease conditions. Relationships between D-amino acids and neurophysiology may involve the significant contribution of D-Serine or D-Aspartate to the synaptic function, including neurotransmission and synaptic plasticity. Gut-microbiota could play important roles in the brain-function, since bacteria in the gut provide a significant contribution to the host pool of D-amino acids. In addition, the alteration of the composition of the gut microbiota might lead to schizophrenia. Furthermore, D-amino acids are known as a physiologically active substance, constituting useful biomarkers of several brain disorders including schizophrenia. In this review, we wish to provide an outline of the roles of D-amino acids in brain health and neuropsychiatric disorders with a focus on schizophrenia, which may shed light on some of the superior diagnoses and/or treatments of schizophrenia., 2022年01月31日, 10, 1, 9, 9, 研究論文（学術雑誌）, 国際誌, 10.3390/diseases10010009
• 査読あり, 英語, Journal of Translational Genetics and Genomics, Roles of gut dysbiosis, anti-proliferative proteins, and post-transcriptional regulation in carcinogenesis, Haruka Sawamura; Kurumi Taniguchi; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, The potentially powerful impact of microbiota has attracted much attention. For example, dysbiosis of the gut microbiota could be linked to various cancers. It is probable that DNA damage and DNA repair impairment due to inflammation from gut dysbiosis would be of importance in carcinogenesis and/or preventing carcinogenesis. In fact, the signature of the gut microbiome has been shown to be associated with responses and/or successful survival rate to certain immune-blockade therapy in several cancers. Conversely, living cells have to cope with the danger of reactive oxygen species (ROS) disturbing the integrity of biomolecules, which can eventually lead to carcinogenesis if otherwise untreated. Gut microbiota could modulate considerable levels of ROS and oxidative damage. Interestingly, an anti-proliferative family (APRO) characterized by several immediate early responsive gene products might be deeply involved in the mechanism of carcinogenesis. It has been described that APRO proteins also participate in a variety of cellular processes including cell division, DNA repair, and mRNA stability. The biological function of APRO proteins seems to be quite complicated; however, they might be a key modulator of microRNAs (miRNAs) for post-transcriptional regulation. The next generation of therapy would likely contain strategies for modifying the redox background as well as the regulation of ROS in cells and/or for better DNA repair machinery with the APRO proteins via the modulation of miRNA-derived post-transcriptional regulation in a sustainable manner. Given the important function of the gut microbiota in balancing the immune network, carcinogenesis could therefore be prevented by suitable gut microbiota via the roles of APRO proteins. Consequently, probiotics might play a key role in the modulation of gut immune system in keeping healthy and/or preventing cancers., 2022年, 6, 157, 168, 研究論文（学術雑誌）, 10.20517/jtgg.2021.57
• 査読あり, 英語, Nutrition Research and Practice, Reduction of oocyte lipid droplets and meiotic failure due to biotin deficiency was not rescued by restoring the biotin nutritional status, Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Yasuko Kitagishi; Satoru Matsuda, BACKGROUND/OBJECTIVES: Oocyte lipid droplets play a crucial role in meiosis and embryo development. Biotin is associated with fatty acid synthesis and is the coenzyme for acetyl-CoA carboxylase (ACC). The effects of a biotin deficiency on the oocyte lipid metabolism remain unknown. This study examined the effects of a biotin deficiency and its replenishment on murine 1) oocyte lipid droplet levels, 2) ovary lipid metabolism, and 3) oocyte meiosis. MATERIALS/METHODS: Mice were divided into 3 groups: control, biotin deficient (BD), and recovery groups. The control and BD groups were fed a control diet or BD diet (0.004 or 0 g biotin/kg), respectively. The recovery group mice were fed a BD diet until day 21, and were then fed the control diet from days 22 to 64. This study then quantified the oocyte lipid droplet levels, assessed the oocyte mitochondrial function, and examined the ability of oocytes to undergo meiosis. Ovarian phosphorylated ACC (p-ACC), lipogenesis, β-oxidation, and ATP production-related genes were evaluated. RESULTS: The BD group showed a decrease in lipid droplets and mitochondrial membrane potential and increased p-ACC levels. In the recovery group, the hepatic biotin concentration, ovarian p-ACC levels, and mitochondrial membrane potential were restored to the control group levels. On the other hand, the quantity of lipid droplets in the recovery group was not restored to the control levels. Furthermore, the percentage of oocytes with meiotic abnormalities was higher in the recovery group than in the control group. CONCLUSIONS: A biotin deficiency reduced the oocyte lipid droplet levels by downregulating lipogenesis. The decreased lipid droplets and increased oocyte meiosis failure were not fully restored, even though the biotin nutrition status and gene expression of lipid metabolism was resumed. These results suggest that a biotin deficiency remains robust and can be long-lasting. Biotin might play a crucial role in maintaining the oocyte quality., 2022年, 16, 3, 314, 314, 研究論文（学術雑誌）, 国際誌, 10.4162/nrp.2022.16.3.314
• 査読あり, 英語, World Journal of Biological Chemistry, Neuroprotection by dipeptidyl-peptidase-4 inhibitors and glucagon-like peptide-1 analogs via the modulation of AKT-signaling pathway in Alzheimer’s disease, Yuka Ikeda; Nozomi Nagase; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Alzheimer's disease (AD) is the most common reason for progressive dementia in the elderly. It has been shown that disorders of the mammalian/mechanistic target of rapamycin (mTOR) signaling pathways are related to the AD. On the other hand, diabetes mellitus (DM) is a risk factor for the cognitive dysfunction. The pathogenesis of the neuronal impairment caused by diabetic hyperglycemia is intricate, which contains neuro-inflammation and/or neurodegeneration and dementia. Glucagon-like peptide-1 (GLP1) is interesting as a possible link between metabolism and brain impairment. Modulation of GLP1 activity can influence amyloid-beta peptide aggregation via the phosphoinositide-3 kinase/AKT/mTOR signaling pathway in AD. The GLP1 receptor agonists have been shown to have favorable actions on the brain such as the improvement of neurological deficit. They might also exert a beneficial effect with refining learning and memory on the cognitive impairment induced by diabetes. Recent experimental and clinical evidence indicates that dipeptidyl-peptidase-4 (DPP4) inhibitors, being currently used for DM therapy, may also be effective for AD treatment. The DPP-4 inhibitors have demonstrated neuroprotection and cognitive improvements in animal models. Although further studies for mTOR, GLP1, and DPP4 signaling pathways in humans would be intensively required, they seem to be a promising approach for innovative AD-treatments. We would like to review the characteristics of AD pathogenesis, the key roles of mTOR in AD and the preventive and/ or therapeutic suggestions of directing the mTOR signaling pathway., 2021年11月27日, 12, 6, 104, 113, 研究論文（学術雑誌）, 国際誌, 10.4331/wjbc.v12.i6.104
• 査読あり, 英語, Recent Progress in Nutrition, Gut Microbiota Potentiates the Effect of Immune Checkpoint Therapy against Cancers, Haruka Sawamura; Kurumi Taniguchi; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Immune checkpoints have been aggressively investigated for anti-cancer immunotherapy. The power of microbiota on the outcome of this immunotherapy has attracted much attention. For example, intestinal microorganisms play a key role in the effectiveness of programmed cell death 1 (PD1) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) blockade. Additionally, short-chain fatty acids produced in the gut may modulate anti-CTLA4 and anti-PD1 stimulated immune responses and their anti-tumor efficacy. Enhancing the anti-tumor effects of CTLA4 blockade depends on specific Bacteroides sp. of the gut microbiota, suggesting novel approaches to improve such immunotherapies. However, the molecular mechanism of the immune-potentiation remains largely unknown. Changes in the microbiota are influenced by dietary and environmental factors. Here, we have suggested the molecular mechanism of action regarding the interplay between gut microbiota and the anti-cancer immune system with APRO family proteins, which might contribute to innovative cancer therapy in the future., 2021年11月16日, 2, 1, 1, 1, 研究論文（学術雑誌）, 10.21926/rpn.2201007
• 査読あり, 英語, Exploration of Medicine, Reactive oxygen species may influence on the crossroads of stemness, senescence, and carcinogenesis in a cell via the roles of APRO family proteins, Yuka Ikeda; Kurumi Taniguchi; Nozomi Nagase; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Excessive reactive oxygen species (ROS) may cause oxidative stress which is involved in aging and in the pathogenesis of various human diseases. Whereas unregulated levels of the ROS may be harmful, regulated basal level of ROS are even necessary to support cellular functions as a second messenger for homeostasis under physiological conditions. Therefore, redox medicine could develop as a new therapeutic concept for human health-benefits. Here, we introduce the involvement of ROS on the crossroads of stemness, senescence, and carcinogenesis in a stem cell and cancer cell biology. Amazingly, the anti-proliferative (APRO) family anti-proliferative proteins characterized by immediate early growth responsive genes may also be involved in the crossroads machinery. The biological functions of APRO proteins (APROs) seem to be quite intricate, however, which might be a key modulator of microRNAs (miRNAs). Given the crucial roles of ROS and APROs for pathophysiological functions, upcoming novel therapeutics should include vigilant modulation of the redox state. Next generation of medicine including regenerative medicine and/or cancer therapy will likely comprise strategies for altering the redox environment with the APROs via the modulation of miRNAs as well as with the regulation of ROS of cells in a sustainable manner., 2021年10月31日, 研究論文（学術雑誌）, 10.37349/emed.2021.00062
• 査読あり, 英語, The American Journal of Pathology, A novel mouse model of non-alcoholic steatohepatitis suggests that liver fibrosis initiates around lipid-laden macrophages, Mayuko Ichimura-Shimizu; Yosuke Tsuchiyama; Yuki Morimoto; Minoru Matsumoto; Tomoko Kobayashi; Satoshi Sumida; Takumi Kakimoto; Takeshi Oya; Hirohisa Ogawa; Michiko Yamashita; Satoru Matsuda; Katsuhisa Omagari; Shu Taira; Koichi Tsuneyama, Various cells such as macrophages and hepatic stellate cells interact in the generation of fibrosis in nonalcoholic steatohepatitis (NASH), but the mechanism remains unclear. We employed a high fat/cholesterol/cholate (HFCC) diet to generate a model of NASH-related fibrosis and investigate the pathogenesis of fibrosis. Two mouse strains differing in susceptibility to obesity, the susceptible strain C57BL/6J (B6) and the relatively resistant strain A/J, developed hepatic histological features of NASH including fat deposition, intralobular inflammation, hepatocyte ballooning, and fibrosis after 9 weeks of HFCC diet feeding. The severity of hepatic inflammation and fibrosis was greater in A/J mice than in B6 mice. A/J mice fed the HFCC diet exhibited characteristic CD204-positive lipid-laden macrophage aggregation in hepatic parenchyma. Polarized light visualized the Maltese cross, namely cholesterol crystals within the aggregated macrophages. Moreover, fibrosis developed in a ring-shape from the periphery of the aggregated macrophages, i.e., the starting point of fibrosis could be visualized histologically. Furthermore, matrix assisted laser desorption/ionization mass spectrometry imaging analysis detected a molecule at m/z 772.462, which corresponds to the protonated ion of phosphatidylcholine (P-18:1 (11Z)/18:0) and phosphatidylethanolamine (18:0/20:2 (11Z, 14Z)), in aggregated macrophages in adjacent to the fibrotic lesions. In conclusion, the present HFCC diet-fed A/J model provides an ideal tool to study fibrogenesis and enables novel insights into the pathophysiology of NASH-related fibrosis., 2021年10月, 研究論文（学術雑誌）, 国際誌, 10.1016/j.ajpath.2021.10.002
• 査読あり, 英語, Reproductive Medicine and Biology, d‐Leucine protects oocytes from chronic psychological stress in mice, Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Yasuko Kitagishi; Satoru Matsuda, Purpose: Psychological stress could negatively influence female reproductive ability. d-Leucine (d-Leu) is a d-type amino acid found in foods and mammalian tissues. We have examined the protective effects of d-Leu on oocyte abnormality induced by psychological stress. Methods: Female mice (6-week-old) were divided into three groups: control, restraint stress (RS), and RS/d-Leu. The RS and RS/d-Leu mice were holed for 3 hours daily during 14 days. RS/d-Leu mice were fed 0.3% d-Leu diet. The oocyte maturation failure was analyzed by shapes of spindles and chromosomes. In addition, levels of heme-oxygenase-1 (HO-1) and superoxide dismutase (SOD) expression in the ovaries were also examined. Whether d-Leu reduces the generation of reactive oxygen species (ROS) in cultured cells, K562 cells were treated with d-Leu, and then ROS in K562 were analyzed. Results: Oocyte maturation failure was increased in RS mice. d-Leu reduced abnormal oocytes to control level. The expression levels of HO-1 and SOD2 increased in RS/d-Leu mice compared to those of RS mice. ROS levels were decreased in K562 cells with d-Leu in a dose-dependent manner. Conclusions: We concluded that d-Leu protects oocytes from psychological stress through the induction of HO-1 and SOD2 expression then by reducing oxidative stress., 2021年10月, 20, 4, 477, 484, 研究論文（学術雑誌）, 国内誌, 10.1002/rmb2.12396
• 査読あり, その他, Oxygen, Comprehension of the Relationship between Autophagy and Reactive Oxygen Species for Superior Cancer Therapy with Histone Deacetylase Inhibitors, Yuka Ikeda; Nozomi Nagase; Ai Tsuji; Kurumi Taniguchi; Yasuko Kitagishi; Satoru Matsuda, Epigenetics contains various mechanisms by which cells employ to regulate the transcription of many DNAs. Histone acetylation is an obvious example of the epigenetic mechanism regulating the expression of several genes by changing chromatin accessibility. Histone deacetylases (HDACs) are a class of enzymes that play a critical role in the epigenetic regulation by deacetylation of histone proteins. Inhibitors of the histone deacetylase could result in hyperacetylation of histones, which eventually induce various cellular consequences such as generation of reactive oxygen species (ROS), activation of apoptotic pathways, and initiating autophagy. In particular, excessive levels of ROS have been proposed to contribute to the pathophysiology of various diseases including cancer. Cancers are, as it were, a class of redox diseases. Low levels of ROS are beneficial for cells, however, cancer cells generally have high levels of ROS, which makes them more susceptible than normal cells to the further increases of ROS levels. Cancer cells exhibit metabolic alterations for managing to sustain these oxidative stresses. There is a growing interest in the use of HDAC inhibitors as promising cancer therapeutics with potentiating the activity of established therapeutic applications. Therefore, it should be important to understand the underlying relationship between the regulation of HDACs, ROS production, and cancer cell biology., 2021年07月25日, 1, 1, 22, 31, 研究論文（学術雑誌）, 10.3390/oxygen1010004
• 査読あり, その他, Academia Letters, COVID-19 and Glaucoma, Satoru Matsuda; Nozomi Nagase; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi, 2021年07月16日, 研究論文（学術雑誌）, 10.20935/al2171
• 査読あり, 英語, Journal of Research in Medical Sciences, COVID-19 cellular pathogenesis in brief, Yuka Ikeda; Ai Tsuji; Mutsumi Murakami; Satoru Matsuda, 2021年, 26, 1, 129, 129, 研究論文（学術雑誌）, 国際誌, 10.4103/jrms.jrms_471_20
• 査読あり, その他, AIMS Bioengineering, Implications of Gut-Brain axis in the pathogenesis of Psychiatric disorders, Kurumi Taniguchi; Yuka Ikeda; Nozomi Nagase; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda,

  <abstract> <p>Psychiatric disorders may extremely impair the quality of life with patients and are important reasons of social disability. Several data have shown that psychiatric disorders are associated with an altered composition of gut microbiota. Dietary intake could determine the microbiota, which contribute to produce various metabolites of fermentation such as short chain fatty acids. Some of the metabolites could result in epigenetic alterations leading to the disease susceptibility. Epigenetic dysfunction is in fact implicated in various psychiatric and neurologic disorders. For example, it has been shown that neuroepigenetic dysregulation occurs in psychiatric disorders including schizophrenia. Several studies have demonstrated that the intestinal microbiome may influence the function of central nervous system. Furthermore, it has been proved that the alterations in the gut microbiota-composition might affect in the bidirectional communication between gut and brain. Similarly, evidences demonstrating the association between psychiatric disorders and the gut microbiota have come from preclinical studies. It is clear that an intricate symbiotic relationship might exist between host and microbe, although the practical significance of the gut microbiota has not yet to be determined. In this review, we have summarized the function of gut microbiota in main psychiatric disorders with respect to the mental health. In addition, we would like to discuss the potential mechanisms of the disorders for the practical diagnosis and future treatment by using bioengineering of microbiota and their metabolites.</p> </abstract>, 2021年, 8, 4, 243, 256, 研究論文（学術雑誌）, 10.3934/bioeng.2021021

• 査読あり, その他, Cells, Reactive Oxygen Species, Superoxide Dimutases, and PTEN-p53-AKT-MDM2 Signaling Loop Network in Mesenchymal Stem/Stromal Cells Regulation., Matsuda S; Nakagawa Y; Kitagishi Y; Nakanishi A; Murai T, 2018年05月, 7, 5, 10.3390/cells7050036
• 査読あり, 英語, JOURNAL OF NUTRITIONAL BIOCHEMISTRY, A diet-induced Sprague-Dawley rat model of nonalcoholic steatohepatitis-related cirrhosis, Mayuko Ichimura; Miki Masuzumi; Miku Kawase; Mika Sakaki; Shizuka Tamaru; Yasuo Nagata; Kazunari Tanaka; Kazuhito Suruga; Koichi Tsuneyama; Satoru Matsuda; Katsuhisa Omagari, Certain modified diets containing saturated fatty acids, cholesterol or fructose lead to the development of nonalcoholic steatohepatitis (NASH)-related fibrosis in rodents; however, progression to cirrhosis is rare. Experimental liver cirrhosis models have relied on genetic manipulation or administration of hepatotoxins. This study aimed to establish a reliable dietary model of NASH-related cirrhosis in a relatively short period. Male Sprague-Dawley rats (9 weeks of age) were randomly assigned to normal, high-fat (HF), or two types (1.25% or 2.5% cholesterol) of high-fat and high-cholesterol (HFC) diets for 18 weeks. All HFC diets contained 2% cholic acid by weight. Histopathological analysis revealed that the HFC diets induced obvious hepatic steatosis, inflammation with hepatocyte ballooning and advanced fibrosis (stage 3-4) in all 12 rats at 27 weeks of age. In contrast, all five rats given the HF diet developed mild steatosis and inflammation without fibrosis. The amount of cholesterol in the liver and hepatocellular mitochondria( and microsomal fractions was significantly higher in rats fed the HFC diets than the normal or HF diets. The HFC diets significantly suppressed mRNA levels of microsomal triglyceride transfer protein, adenosine triphosphate binding cassette transporter G5, bile acid CoA: amino acid N-acyltransferase and bile salt export pump, as well as the enzymatic activity of carnitine palmitoyltransferase in the liver. In conclusion, the HFC diets induced liver cirrhosis in conjunction with hepatic features of NASH in Sprague-Dawley rats within 18 weeks, and altered gene expression and enzyme activity to accumulate lipid and bile acid in the liver. (C) 2016 Elsevier Inc. All rights reserved., 2017年02月, 40, 62, 69, 研究論文（学術雑誌）, 10.1016/j.jnutbio.2016.10.007
• 査読あり, 英語, Journal of Clinical Investigation, Cardiac myofibroblast engulfment of dead cells facilitates recovery after myocardial infarction, Nakaya, M.; Watari, K.; Tajima, M.; Nakaya, T.; Matsuda, S.; Ohara, H.; Nishihara, H.; Yamaguchi, H.; Hashimoto, A.; Nishida, M.; Nagasaka, A.; Horii, Y.; Ono, H.; Iribe, G.; Inoue, R.; Tsuda, M.; Inoue, K.; Tanaka, A.; Kuroda, M.; Nagata, S.; Kurose, H., Myocardial infarction (MI) results in the generation of dead cells in the infarcted area. These cells are swiftly removed by phagocytes to minimize inflammation and limit expansion of the damaged area. However, the types of cells and molecules responsible for the engulfment of dead cells in the infarcted area remain largely unknown. In this study, we demonstrated that cardiac myofibroblasts, which execute tissue fibrosis by producing extracellular matrix proteins, efficiently engulf dead cells. Furthermore, we identified a population of cardiac myofibroblasts that appears in the heart after MI in humans and mice. We found that these cardiac myofibroblasts secrete milk fat globule-epidermal growth factor 8 (MFG-E8), which promotes apoptotic engulfment, and determined that serum response factor is important for MFG-E8 production in myofibroblasts. Following MFG-E8-mediated engulfment of apoptotic cells, myofibroblasts acquired antiinflammatory properties. MFG-E8 deficiency in mice led to the accumulation of unengulfed dead cells after MI, resulting in exacerbated inflammatory responses and a substantial decrease in survival. Moreover, MFG-E8 administration into infarcted hearts restored cardiac function and morphology. MFG-E8-producing myofibroblasts mainly originated from resident cardiac fibroblasts and cells that underwent endothelial-mesenchymal transition in the heart. Together, our results reveal previously unrecognized roles of myofibroblasts in regulating apoptotic engulfment and a fundamental importance of these cells in recovery from MI., 2017年, 127, 1, 383, 401, 研究論文（学術雑誌）, 国際誌, 10.1172/JCI83822
• 英語, Biochimica et biophysica acta, Molecular cloning and characterization of a novel human gene (NESCA) which encodes a putative adapter protein containing SH3., S Matsuda; K Miyazaki; Y Ichigotani; H Kurata; Y Takenouchi; T Yamamoto; Y Nimura; T Irimura; S Nakatsugawa; M Hamaguchi, A full-length cDNA encoding a novel protein was isolated and sequenced from a human placental cDNA library. This cDNA consists of 1990 bp and has a predicted open reading frame encoding 433 amino acids. It possesses an Src homology 3 (SH3) motif, a leucine zipper motif and no catalytic domain, suggesting that it seems to be an adapter protein. PCR-based mapping with both a monochromosomal hybrid panel and radiation hybrid cell panels placed the gene to human chromosome 1q21-22., 2000年04月25日, 1491, 1-3, 321, 6, 研究論文（学術雑誌）, 国際誌
• 英語, Biochimica et biophysica acta, Molecular cloning and characterization of a novel human gene (HERNA) which encodes a putative RNA-helicase., S Matsuda; Y Ichigotani; T Okuda; T Irimura; S Nakatsugawa; M Hamaguchi, A full-length cDNA encoding a novel protein was isolated and sequenced from a human hepatocellular cDNA library. This cDNA consists of 7037 base pairs and has a predicted open reading frame encoding 1924 amino acids. It possesses an RNA-helicase motif containing a DEXH-box in its amino-terminus and an RNase motif in the carboxy-terminus. From a striking homology to Caenorhabditis elegans K12H4.8, it might be a human homolog of the K12H4.8. PCR-based mapping with both a monochromosomal hybrid panel and radiation hybrid cell panels placed the gene to human chromosome 14q31 near the marker D14S605., 2000年01月31日, 1490, 1-2, 163, 9, 研究論文（学術雑誌）, 国際誌
• 査読あり, 英語, JOURNAL OF IMMUNOLOGY, Physical and functional interactions of protein tyrosine kinases, p59(fyn) and ZAP-70, in T cell signaling, Noemi Fusaki; Satoru Matsuda; Hirofumi Nishizumi; Hisashi Umemori; Tadashi Yamamoto, The src family protein tyrosine kinases participate in signaling through cell surface receptors that lack intrinsic tyrosine kinase domains, One of the src family kinases, p59(fyn)(Fyn), plays an important role in the TCR-mediated signaling, Here we report that Fyn becomes associated with the zeta-associated tyrosine kinase, ZAP-70, in a T cell hybridoma upon stimulation, The association was transient; it occurred as early as 10 s after stimulation and disappeared after 10 min. The two proteins were also associated with each other when coexpressed in COS cells, Coexpression of the zeta-chain was not required for their interaction, Mutational analysis of Fyn and ZAP-70 revealed that their kinase activities were relevant to the association, Deletion of both the SH2 and SH3 domains of Fyn resulted in the decrease of the association with ZAP-70, Consistently, Fyn-SH2 and Fyn-SH3 fused to glutathione S-transferase were able to bind to ZAP-70, These data suggest that multiple sites of Fyn and ZAP-70 are involved in the association, Furthermore, coexpression of the wild-type of both kinases in COS cells enhanced tyrosine phosphorylation of the helix-turn-helix-containing protein, HS1, HS1 was also tyrosine phosphorylated upon TCR stimulation, Thus, we propose that Fyn phosphorylates and activates ZAP-70 and that both kinases cooperate in TCR signaling., 1996年02月, 156, 4, 1369, 1377, 研究論文（学術雑誌）
• 査読あり, 英語, Experimental Hematology, A new bioassay for human granulocyte colony-stimulating factor (hG-CSF) using murine myeloblastic NFS-60 cells as targets and estimation of its levels in sera from normal healthy persons and patients with infectious and hematological disorders, Shirafuji, N.; Asano, S.; Matsuda, S.; Watari, K.; Takaku, F.; Nagata, S., 1989年, 17, 2, 116, 119, 研究論文（学術雑誌）
• 英語, Non-coding RNA, CircRNAs and RNA-Binding Proteins Involved in the Pathogenesis of Cancers or Central Nervous System Disorders., Yuka Ikeda; Sae Morikawa; Moeka Nakashima; Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Naoko Suga; Ai Tsuji; Satoru Matsuda, Circular RNAs (circRNAs), a newly recognized group of noncoding RNA transcripts, have established widespread attention due to their regulatory role in cell signaling. They are covalently closed noncoding RNAs that form a loop, and are typically generated during the splicing of precursor RNAs. CircRNAs are key post-transcriptional and post-translational regulators of gene expression programs that might influence cellular response and/or function. In particular, circRNAs have been considered to function as sponges of specific miRNA, regulating cellular processes at the post-transcription stage. Accumulating evidence has shown that the aberrant expression of circRNAs could play a key role in the pathogenesis of several diseases. Notably, circRNAs, microRNAs, and several RNA-binding proteins, including the antiproliferative (APRO) family proteins, could be indispensable gene modulators, which might be strongly linked to the occurrence of diseases. In addition, circRNAs have attracted general interest for their stability, abundance in the brain, and their capability to cross the blood-brain barrier. Here, we present the current findings and theragnostic potentials of circRNAs in several diseases. With this, we aim to provide new insights to support the development of novel diagnostic and/or therapeutic strategies for these diseases., 2023年03月31日, 9, 2, 研究論文（学術雑誌）, 国際誌, 10.3390/ncrna9020023
• 英語, International journal of molecular sciences, The Tryptophan and Kynurenine Pathway Involved in the Development of Immune-Related Diseases., Ai Tsuji; Yuka Ikeda; Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Sae Morikawa; Moeka Nakashima; Tomoko Asai; Satoru Matsuda, The tryptophan and kynurenine pathway is well-known to play an important role in nervous, endocrine, and immune systems, as well as in the development of inflammatory diseases. It has been documented that some kynurenine metabolites are considered to have anti-oxidative, anti-inflammatory, and/or neuroprotective properties. Importantly, many of these kynurenine metabolites may possess immune-regulatory properties that could alleviate the inflammation response. The abnormal activation of the tryptophan and kynurenine pathway might be involved in the pathophysiological process of various immune-related diseases, such as inflammatory bowel disease, cardiovascular disease, osteoporosis, and/or polycystic ovary syndrome. Interestingly, kynurenine metabolites may be involved in the brain memory system and/or intricate immunity via the modulation of glial function. In the further deliberation of this concept with engram, the roles of gut microbiota could lead to the development of remarkable treatments for the prevention of and/or the therapeutics for various intractable immune-related diseases., 2023年03月17日, 24, 6, 研究論文（学術雑誌）, 国際誌, 10.3390/ijms24065742
• 英語, International journal of molecular sciences, Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy., Ai Tsuji; Sayuri Yoshikawa; Yuka Ikeda; Kurumi Taniguchi; Haruka Sawamura; Sae Morikawa; Moeka Nakashima; Tomoko Asai; Satoru Matsuda, Mitophagy/autophagy plays a protective role in various forms of liver damage, by renovating cellular metabolism linking to sustain liver homeostasis. A characterized pathway for mitophagy is the phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkin-dependent signaling pathway. In particular, PINK1-mediated mitophagy could play an indispensable role in improving the metabolic dysfunction-associated fatty liver disease (MAFLD) which could precede to steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma. In addition, the PI3K/AKT/mTOR pathway might regulate the various characteristics of cellular homeostasis including energy metabolism, cell proliferation, and/or cell protection. Therefore, targeting mitophagy with the alteration of PI3K/AKT/mTOR or PINK1/Parkin-dependent signaling to eliminate impaired mitochondria might be an attractive strategy for the treatment of MAFLD. In particular, the efficacy of prebiotics for the treatment of MAFLD has been suggested to be useful via the modulation of the PI3K/AKT/mTOR/AMPK pathway. Additionally, several edible phytochemicals could activate mitophagy for the improvement of mitochondrial damages, which could also be a promising option to treat MAFLD with providing liver protection. Here, the potential therapeutics with several phytochemicals has been discussed for the treatment of MAFLD. Tactics with a viewpoint of prospective probiotics might contribute to the development of therapeutic interventions., 2023年03月13日, 24, 6, 研究論文（学術雑誌）, 国際誌, 10.3390/ijms24065465

MISC

• 査読あり, 英語, International Journal of Molecular Sciences, MDPI AG, Neuron membrane trafficking and protein kinases involved in autism and ADHD, Yasuko Kitagishi; Akari Minami; Atsuko Nakanishi; Yasunori Ogura; Satoru Matsuda, A brain-enriched multi-domain scaffolding protein, neurobeachin has been identified as a candidate gene for autism patients. Mutations in the synaptic adhesion protein cell adhesion molecule 1 (CADM1) are also associated with autism spectrum disorder, a neurodevelopmental disorder of uncertain molecular origin. Potential roles of neurobeachin and CADM1 have been suggested to a function of vesicle transport in endosomal trafficking. It seems that protein kinase B (AKT) and cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) have key roles in the neuron membrane trafficking involved in the pathogenesis of autism. Attention deficit hyperactivity disorder (ADHD) is documented to dopaminergic insufficiencies, which is attributed to synaptic dysfunction of dopamine transporter (DAT). AKT is also essential for the DAT cell-surface redistribution. In the present paper, we summarize and discuss the importance of several protein kinases that regulate the membrane trafficking involved in autism and ADHD, suggesting new targets for therapeutic intervention., 2015年01月30日, 16, 2, 3095, 3115, 書評論文,書評,文献紹介等, 10.3390/ijms16023095
• 査読あり, 英語, International Journal of Molecular Medicine, Spandidos Publications, PI3K/AKT/PTEN pathway as a target for Crohn's disease therapy (Review), Nana Tokuhira; Yasuko Kitagishi; Miho Suzuki; Akari Minami; Atsuko Nakanishi; Yuna Ono; Keiko Kobayashi; Satoru Matsuda; Yasunori Ogura, The pathogenesis of inflammatory bowel disease (IBD), including Crohn's disease, is a subject of increasing interest. Loss-of-function mutations in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) are strong genetic factors linked to Crohn's disease, which eventually leads to an excessive mucosal inflammatory response directed against components of normal gut microbiota. Reactive oxygen species (ROS) play an important role in inflammation processes, as well as in transduction of signals from receptors for several cytokines, such as tumor necrosis factor α (TNFα). ROS activate nuclear factor-κB (NF-κB) via IκB kinase (IKK) through the PI3K/AKT/PTEN pathway. Therefore, this pathway is recognized to play a key role in Crohn's disease. Loss of function has been demonstrated to occur as an early event in a wide variety of diseases. Given this prevalent involvement in a number of diseases, the molecular development that modulates this pathway has been the subject of several studies. In addition, it has been the focus of extensive research and drug discovery activities. A better understanding of the molecular assemblies may reveal novel targets for the therapeutic development against Crohn's disease., 2015年01月01日, 35, 1, 10, 16, 書評論文,書評,文献紹介等, 10.3892/ijmm.2014.1981
• 査読あり, 英語, International Journal of Oncology, Defective DNA repair systems and the development of breast and prostate cancer (Review), Yasuko Kitagishi; Mayumi Kobayashi; Satoru Matsuda, Genetic defects in DNA repair and DNA damage response genes often lead to an increase in cancer incidence. The role of defects is also associated with the modulation of hormone signaling pathways. A number of studies have suggested a role for estrogen in the regulation of DNA repair activity. Furthermore, mutations or epigenetic silencing in DNA repair genes have been associated with the sensitivity of cancers to hormonal therapy. The molecular basis for the progression of cancers from hormone-dependent to hormone-independent remains a critical issue in the management of these types of cancer. In the present review, we aimed to summarize the function of DNA repair molecules from the viewpoint of carcinogenesis and hormone-related cell modulation, providing a comprehensive view of the molecular mechanisms by which hormones may exert their effects on the regulation of tumor progression., 2013年01月, 42, 1, 29, 34, 書評論文,書評,文献紹介等, 10.3892/ijo.2012.1696
• 査読無し, 日本語, ビタミン, 公益社団法人 日本ビタミン学会, ヒト白血球培養細胞におけるグルタミン酸デカルボキシラーゼの発現様式の解析, 植野 洋志; 菊田 香苗; 通山 由美; 松川 聡子; 松田 覚; 赤桐 里美, Expression of GAD65, an isoform of glutamate decarboxylase, was examined on peripheral blood mononuclear leukocyte (PBMC) and on three kinds of mononuclear leukocyte cell lines, Jurkat, Ramos and HL-60. RT-PCR was performed for mRNA isolated from each cells with the probes specific to GAD65. PBMC and mononuclear leukocyte cell lines were found to give an mRNA corresponding to the full length of GAD65. Western blot analysis was carried out for each cell extracts by using GAD specific antibodies. Protein band at 80 kDa was found for PBMC that was different from 60 kDa found for each cell lines, where those protein bands were recognized by different antibodies. Results show that PBMC and mononuclear leukocyte cell lines express full length mRNA of GAD65 and GAD65 of mononuclear leukocytes differ in pattern of expression., 2013年, 87, 3, 147, 151, 10.20632/vso.87.3_147
• 査読あり, 英語, Journal of Oncology, Protection against cancer with medicinal herbs via activation of tumor suppressor, Yasuko Kitagishi; Mayumi Kobayashi; Satoru Matsuda, Cancer remains a major cause of death, although research is ongoing for the development of more effective drugs. Some herbs have shown potential in preventing the occurrence and/or progression of cancer and other chronic diseases. They are being screened comprehensively to explore the possibility of development of feasible anticancer drugs. However, more information is required about the response to and the molecular target for specific herbs. It seems that there is a relationship between some medicinal herbs and tumor suppressor molecules which protect a cell from cancer. In this paper, we summarize the progress of recent research on herbs, with a particular focus on its anticancer role and molecular mechanisms underlying the cancer prevention property, supporting design for further research in this field. © 2012 Yasuko Kitagishi et al., 2012年, 書評論文,書評,文献紹介等, 10.1155/2012/236530
• 査読あり, 英語, FEBS LETTERS, ELSEVIER SCIENCE BV, In search of a function for the TIS21/PC3/BTG1/TOB family, S Matsuda; JP Rouault; JP Magaud; C Berthet, The Btg family of anti-proliferative gene products includes Pc3/Tis21/Btg2, Btg1, Tob, Tob2, Ana/Btg3, Pc3k and others. These proteins are characterized by similarities in their amino-terminal region: the Btg1 homology domain. However, the pleiotropic nature of these family proteins has been observed and no common physiological function among family members was suggested from the history of their identification. Recent progress in the search for Btg family functions has come from the analysis of cell regulation and of cell differentiation. It is now emerging that every member of this family has a potential to regulate cell growth. We would like to propose here to use a nomenclature APRO as a new term for the family. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B,V, All rights reserved., 2001年05月, 497, 2-3, 67, 72, 書評論文,書評,文献紹介等
• 査読あり, 英語, BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, ELSEVIER SCIENCE BV, Molecular cloning and characterization of a novel human gene (NESCA) which encodes a putative adapter protein containing SH3, S Matsuda; K Miyazaki; Y Ichigotani; H Kurata; Y Takenouchi; T Yamamoto; Y Nimura; T Irimura; S Nakatsugawa; M Hamaguchi, A full-length cDNA encoding a novel protein was isolated and sequenced from a human placental cDNA library. This cDNA consists of 1990 bp and has a predicted open reading frame encoding 433 amino acids. It possesses an Src homology 3 (SH3) motif, a leucine zipper motif and no catalytic domain, suggesting that it seems to be an adapter protein. PCR-based mapping with both a monochromosomal hybrid panel and radiation hybrid cell panels placed the gene to human chromosome 1q21-22. (C) 2000 Elsevier Science B.V. All rights reserved., 2000年04月, 1491, 1-3, 321, 326
• 査読あり, 英語, CANCER RESEARCH, AMER ASSOC CANCER RESEARCH, Molecular cloning and characterization of human MAWD, a novel protein containing WD-40 repeats frequently overexpressed in breast cancer, S Matsuda; R Katsumata; T Okuda; T Yamamoto; K Miyazaki; T Senga; K Machida; AA Thant; S Nakatsugawa; M Hamaguchi, A full-length cDNA clone encoding a novel protein containing WD-40 repeats, which were frequently involved in protein-protein interactions, was isolated and-sequenced. This clone had a predicted open reading frame (ORF) encoding 350 amino acids possessing six repeats of WD-40 motif, It was most closely homologous to TRIP-1, a phosphorylation substrate of the transforming growth factor-beta type II receptor. In the process of characterizing the function of the new gene product, we found that overexpression of the gene seemed to activate mitogen-activated protein kinase and to promote anchorage-independent growth of the cells, Moreover, the gene product was frequently overexpressed in human tumor breast tissues compared with their normal breast tissues, suggesting that the gene might be involved in the tumor progression, Radiation hybrid mapping placed the gene into human chromosome 12q11-12 near the marker D12S1593., 2000年01月, 60, 1, 13, 17
• 査読あり, 英語, BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, ELSEVIER SCIENCE BV, Molecular cloning and characterization of a novel human gene (HERNA) which encodes a putative RNA-helicase, S Matsuda; Y Ichigotani; T Okuda; T Irimura; S Nakatsugawa; M Hamaguchi, A full-length cDNA encoding a novel protein was isolated and sequenced from a human hepatocellular cDNA library. This cDNA consists of 7037 base pairs and has a predicted open reading frame encoding 1924 amino acids. It possesses an RNA-helicase motif containing a DEXH-box in its amino-terminus and an RNase motif in the carboxy-terminus. From a striking homology to Caenorhabditis elegans K12H4.8, it might be a human homolog of the K12H4.8. PCR-based mapping with both a monochromosomal hybrid panel and radiation hybrid cell panels placed the gene to human chromosome 14q31 near the marker D14S605. (C) 2000 Elsevier Science B.V. All rights reserved., 2000年01月, 1490, 1-2, 163, 169
• 査読無し, 日本語, 日本癌学会総会記事, c‐Src及びv‐SrcのSH3ドメイン 癌化能・基質特異性の比較, 宮崎耕; 松田覚; 二村雄次; 浜口道成, 1999年08月30日, 58th, 521, 521
• 査読無し, 日本語, 臨床検査, 遺伝子診断 Srcチロシンキナーゼ, 松田覚; 宮崎耕; 浜口道成, 1999年01月, 43, 1, 75, 80, 10.11477/mf.1542903986
• 査読無し, 日本語, 環境科学会年会一般講演・シンポジウム・プログラム, 紫外線・重金属等の環境変動の細胞内情報伝達に重要な役割を担っているチロシンキナーゼの環境科学的意義, 松田覚; 浜口道成, 1997年, 1997, 224, 225
• 査読あり, 英語, ONCOGENE, STOCKTON PRESS, Tob, a novel protein that interacts with p185(erbB2), is associated with antiproliferative activity, S Matsuda; J KawamuraTsuzuku; M Ohsugi; M Yoshida; M Emi; Y Nakamura; M Onda; Y Yoshida; A Nishiyama; T Yamamoto, We have molecularly cloned a cDNA for a novel protein termed Tob (Transducer of ErbB-2) that interacts with the c-erbB-2 gene product p185(erbB2). Nucleotide sequencing reveals that the Tob protein is a 45 kDa protein that does not contain either SH2 (Src Homology 2) or SH3 domain but is homologous to the previously characterized anti-proliferative gene product BTG-1 at its amino-terminal half. The carboxyl-terminal half of Tob is characterized by the presence of a sequence rich in proline and glutamine and shows no homology to known proteins. Like BTG-1, exogenously expressed Tob is able to suppress growth of NIH3T3 cells, but the growth suppression is hampered by the presence of kinase-active p185(erbB2). By using the GST-Tob protein that contains either full length or amino-terminal half of Tob, we show that the carboxyl-terminal half of Tob is relevant to its interaction with p185(erbB2). Furthermore, we could co-immunoprecipitate the Tob protein with anti-ErbB-2 antibody, and reciprocally the p185(erbB2). With anti-Tob antibodies. These data suggest that p185(erbB2) negatively regulates the Tob-mediated anti-proliferative pathway through its interaction with Tob, resulting possibly in growth stimulation by p185(erbB2). Finally, expression of the Tob mRNA is observed in various cell types and is not correlated with expression of c-erbB-2, suggesting that other receptor-type protein-tyrosine kinases are also involved in the Tob-mediated regulation of cell growth., 1996年02月, 12, 4, 705, 713
• 査読無し, 日本語, 日本生化学会大会(Web), (公社)日本生化学会, ヒト白血球とその培養細胞におけるグルタミン酸デカルボキシラーゼに関する研究, 菊田香苗; 通山由美; 松川聡子; 松田覚; 赤桐里美; 植野洋志, 2012年12月, 85th, 3P-291 (WEB ONLY), 291
• 日本語, ビタミン, 日本ビタミン学会, 2-V-5 ヒト白血球培養細胞におけるグルタミン酸デカルボキシラーゼの発現様式の解析(一般演題要旨,日本ビタミン学会第64回大会講演要旨), 菊田 香苗; 松川 聡子; 通山 由美; 松田 覚; 赤桐 里美; 植野 洋志, 2012年04月25日, 86, 4, 269, 269
• 査読無し, 日本語, 生化学, (公社)日本生化学会, グルタミン酸デカルボキシラーゼ(GAD)の選択的スプライシング機構の解明, 菊田香苗; 松川聡子; 通山由美; 松田覚; 赤桐里美; 植野洋志, 2011年09月, 84回, ROMBUNNO.4P-0409, 0409
• 査読無し, 英語, CANCER RESEARCH, AMER ASSOC CANCER RESEARCH, Invasion activating caveolin-1 mutation in human scirrhous breast cancers, K Hayashi; S Matsuda; K Machida; T Yamamoto; Y Fukuda; Y Nimura; T Hayakawa; M Hamaguchi, We looked for mutations in the caveolin-1 gene, encoding a critical molecule for membrane signaling to cell growth, in 92 primary human breast cancers, and we report here the identification of a mutation in caveolin-1 at codon 132 (P132L) in 16% of cases. The mutation-positive cases were mostly invasive scirrhous carcinomas. In cell lines expressing the same mutant of caveolin-1, we observed that the mutant Caveolin-1 expression seemed to induce cellular transformation and activation of mitogen-activated protein kinase-signaling pathway and to promote invasion-ability as well as altered actin networks in the cells, These results provide, for the first time, genetic evidence that a functioning Caveolin-1 mutation may have a role in the malignant progression of human breast cancer., 2001年03月, 61, 6, 2361, 2364
• 査読無し, 英語, BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, ELSEVIER SCIENCE BV, Isolation and characterization of a novel human gene (NESH) which encodes a putative signaling molecule similar to e3B1 protein, K Miyazaki; S Matsuda; Y Ichigotani; Y Takenouchi; K Hayashi; Y Fukuda; Y Nimura; M Hamaguchi, Using a conventional cloning technique, a novel full-length cDNA was isolated and sequenced from a human placental cDNA library. This cDNA consists of 2129 bp and has a predicted open reading frame encoding 366 amino acids. It possesses a Src homology 3 (SH3) motif, proline-rich region, serine-rich region and no catalytic domain, suggesting that it seems to be a signaling protein most similar to e3B1, an eps8 SH3 binding protein. PCR-based mapping with both a monochromosomal hybrid panel and radiation hybrid cell panels placed the gene to human chromosome 17q21.3 near the marker D17S1795. (C) 2000 Elsevier Science B.V. All rights reserved., 2000年09月, 1493, 1-2, 237, 241, 10.1016/S0167-4781(00)00158-5
• 査読無し, 英語, ONCOGENE, STOCKTON PRESS, v-Src suppresses SHPS-1 expression via the Ras-MAP kinase pathway to promote the oncogenic growth of cells, K Machida; S Matsuda; K Yamaki; T Senga; AA Thant; H Kurata; K Miyazaki; K Hayashi; T Okuda; T Kitamura; T Hayakawa; M Hamaguchi, We investigated the effect of cell transformation by v-src on the expression and tyrosine phosphorylation of SHPS-1, a putative docking protein for SHP-1 and SHP-2. We found that transformation by v-sle virtually inhibited the SHPS-1 expression at mRNA level. While nontransforming Src kinases including c-Src, nonmyristoylated forms of v-Src had no inhibitory effect on SHPS-1 expression, transforming Src kinases including wild-type v-Src and chimeric mutant of c-Src bearing v-Src SH3 substantially suppressed the SHPS-1 expression. In cells expressing temperature sensitive mutant of v-Src, suppression of the SHPS-1 expression was temperature-dependent. In contrast, tyrosine phosphorylation of SHPS-1 was rather activated in cells expressing c-Src or nonmyristoylated forms of v-Src, SHPS-1 expression in SR3Y1 was restored by treatment with herbimycin A, a potent inhibitor of tyrosine kinase, or by the expression of dominant negative form of Ras. Contrary, active form of Mek1 markedly suppressed SHPS-1 expression. Finally, overexpression of SHPS-1 in SR3Y1 led to the drastic reduction of anchorage independent growth of the cells. Taken together, our results suggest that the suppression of SHPS-1 expression is a pivotal event for cell transformation by v-src, and the Ras-MAP kinase cascade plays a critical role in the suppression., 2000年03月, 19, 13, 1710, 1718, 10.1038/sj.onc.1203497
• 査読あり, 英語, MOLECULAR BIOLOGY OF THE CELL, AMER SOC CELL BIOLOGY, Regulation of the biochemical properties of Tob by means of its phosphorylation, T Suzuki; J Tsuzuku; Y Yoshida; S Matsuda; T Yamamoto, 1998年11月, 9, 360A, 360A, 記事・総説・解説・論説等（学術雑誌）
• 日本語, ホルモンと臨牀, ストロイドホルモンの膜作用 - エストロゲンによる受容体型チロシンキナーゼErbB-2の活性化 -, 松田 覚; 山本 雅, 1995年05月01日, 43, 5, 49, 52
• 査読無し, 英語, EUROPEAN JOURNAL OF CANCER, PERGAMON-ELSEVIER SCIENCE LTD, Application of a novel growth suppressing gene, tob, for gene therapy of pancreatic cancer in vitro, H Yanagie; H Sumimoto; S Matsuda; Hirose, I; S Hanada; M Eriguchi; K Tani; T Yamamoto; S Asano; T Muto, 1997年09月, 33, 382, 382, 研究発表ペーパー・要旨（国際会議）
• 査読無し, 英語, CANCER GENE THERAPY, APPLETON & LANGE, Inhibition of human pancreatic cancer growth by a novel growth suppressing gene, tob, in vitro, H Yanagie; H Sumimoto; Y Nonaka; S Matsuda; K Tani; T Yamamoto; S Asano; T Muto; M Eriguchi, 1997年09月, 4, 5, 300, 300, 研究発表ペーパー・要旨（国際会議）

書籍等出版物

• 食物科学概論, 朝倉書店, 松田覚 他, 分担, 2014年03月, 日本語, 査読無し, その他
• 高校生物基礎, 実教出版, 松田覚, 監修, 2012年01月, 日本語, 査読無し, その他
• 未来を拓く理数教育への挑戦―奈良女子大学附属中等教育学校, 文理閣, 松田覚; 吉田 信也, 編集, 2010年07月, 日本語, 査読無し, その他
• 恋愛食ー賢い女子中高生のための食育, 久美, 松田覚他, 編集, 2006年02月, 日本語, 査読無し, その他
• 食 up to date, 金芳堂, 松田覚, 2005年01月, 日本語, 査読無し, その他

共同研究・競争的資金等の研究課題

• 2001年, RNA干渉を応用したヒト疾患の予防と治療, 0, 0, 0, 競争的資金
• 2001年, Medical application of RNAi to the human health, 0, 0, 0, 競争的資金