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Affiliation |
Graduate School of Medicine Doctorial Course in Medicine Organ Function-Oriented Medicine Department of Integrative Physiology |
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Mail Address |
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NUMATA Tomohiro
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Graduating School 【 display / non-display 】
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-2001.03
Tokyo Gakugei University Graduated
Graduate School 【 display / non-display 】
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-2006.03
The Graduate University for Advanced Studies Doctor's Course Completed
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-2003.03
Tokyo Gakugei University Graduate School, Division of Education Master's Course Completed
Campus Career 【 display / non-display 】
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2021.10-Now
Akita University Graduate School of Medicine Doctorial Course in Medicine Organ Function-Oriented Medicine Department of Integrative Physiology Professor
External Career 【 display / non-display 】
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2021.10
Akita University Graduate School of Medicine Doctoral Course in Medicine Professor
Research Areas 【 display / non-display 】
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Life Science / Physiology
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Life Science / Animal life science
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Life Science / Applied biochemistry
Thesis for a degree 【 display / non-display 】
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TRPM7 is mechanosensitive volume-regulatory cation channel in human epithelial cells
Tomohiro Numata
2006.03 [Refereed]
Single author
Research Achievements 【 display / non-display 】
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Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7.
Yasunobu Okada, Tomohiro Numata, Ravshan Z Sabirov, Makiko Kashio, Peter G Merzlyak, Kaori Sato-Numata
Frontiers in cell and developmental biology 11 1246955 - 1246955 2023
Research paper (journal)
Cell volume regulation (CVR) is a prerequisite for animal cells to survive and fulfill their functions. CVR dysfunction is essentially involved in the induction of cell death. In fact, sustained normotonic cell swelling and shrinkage are associated with necrosis and apoptosis, and thus called the necrotic volume increase (NVI) and the apoptotic volume decrease (AVD), respectively. Since a number of ubiquitously expressed ion channels are involved in the CVR processes, these volume-regulatory ion channels are also implicated in the NVI and AVD events. In Part 1 and Part 2 of this series of review articles, we described the roles of swelling-activated anion channels called VSOR or VRAC and acid-activated anion channels called ASOR or PAC in CVR and cell death processes. Here, Part 3 focuses on therein roles of Ca2+-permeable non-selective TRPM2 and TRPM7 cation channels activated by stress. First, we summarize their phenotypic properties and molecular structure. Second, we describe their roles in CVR. Since cell death induction is tightly coupled to dysfunction of CVR, third, we focus on their participation in the induction of or protection against cell death under oxidative, acidotoxic, excitotoxic, and ischemic conditions. In this regard, we pay attention to the sensitivity of TRPM2 and TRPM7 to a variety of stress as well as to their capability to physicall and functionally interact with other volume-related channels and membrane enzymes. Also, we summarize a large number of reports hitherto published in which TRPM2 and TRPM7 channels are shown to be involved in cell death associated with a variety of diseases or disorders, in some cases as double-edged swords. Lastly, we attempt to describe how TRPM2 and TRPM7 are organized in the ionic mechanisms leading to cell death induction and protection.
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YOSHINO Masami, KATSUKI Tomoaki, ASAHI Shunsuke, NUMATA Tomohiro, MATSUKAWA Masaki, HARADA Kazuo, HASEGAWA Tadashi
Bulletin of Tokyo Gakugei University. Division of natural sciences 75 63 - 75 2023.09
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The regulation mechanisms of mitochondrial Ca<sup>2+</sup> signaling mediated by cardiac Sigma-1 receptor
Tagashira Hideaki, Shinoda Yasuharu, Numata Tomohiro, Fukunaga Kohji
Proceedings for Annual Meeting of The Japanese Pharmacological Society ( Japanese Pharmacological Society ) 96 1-B-P-020 2022
Cardiovascular disease (CVD) is a leading cause of death worldwide. We previously reported that the Sigma-1 receptor (Sigmar1) is down-regulated in mice with cardiac dysfunction. Recent study suggested that Sigmar1 deficient mice display cardiac dysfunction via impairment of mitochondrial function. However, the mechanism of mitochondrial quality control mediated by Sigmar1 has not been investigated in detail. In this study, we investigated the role of Sigmar1 for ER-mitochondrial tethering and mitochondrial Ca<sup>2+</sup> signaling using a Sigmar1-knockdown cardiomyocytes. We found that disruption of ER-mitochondrial tethering and reduction of ER-mitochondrial Ca<sup>2+</sup> transport was induced by Sigmar1 knockdown in cardiomyocytes. We also demonstrated that Endothelin-1-induced cardiomyocyte hypertrophy is aggravated associated with induction of mitophagy in Sigmar1 knockdown cardiomyocytes. These data suggest that reduction of cardiac Sigmar1 is involved in myocyte hypertrophy by maintaining of intracellular Ca<sup>2+</sup> signaling mediated by regulation of ER-mitochondrial tethering.
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Numata T, Sato-Numata K, Okada Y
Scientific reports 9 ( 1 ) 15554 - 15554 2019.10
◆Original paper【 display / non-display 】
◆Other【 display / non-display 】
Grant-in-Aid for Scientific Research 【 display / non-display 】
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Grant-in-Aid for Scientific Research(C)
Project Year： 2022.04 - 2025.03
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Grant-in-Aid for Scientific Research(C)
Project Year： 2021.04 - 2024.03
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Optical control of the plasma membrane functions by using dynamic exciton
Grant-in-Aid for Transformative Research Areas (A)
Project Year： 2020.11 - 2025.03
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Elucidation of hepatocyte volume regulation and liver regeneration mechanism through TRPM2 activity.
Grant-in-Aid for Scientific Research(C)
Project Year： 2018.04 - 2021.03 Investigator(s): Numata Tomohiro
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Grant-in-Aid for Scientific Research(B)
Project Year： 2015.04 - 2019.03 Investigator(s): Inoue Ryuji