SATO-NUMATA Kaori

写真a

Affiliation

Graduate School of Medicine  Doctorial Course in Medicine  Organ Function-Oriented Medicine  Department of Integrative Physiology
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Research Interests 【 display / non-display 】

  • cell physiology

  • osmotic-sensor

  • cell volume regulation

  • arginine-vasopressin

  • 視床下部

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Graduating School 【 display / non-display 】

  • 2002.04
    -
    2006.03

    Tokyo Gakugei University     Graduated

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Graduate School 【 display / non-display 】

  • 2006.04
    -
    2011.03

    The Graduate University for Advanced Studies    Doctor's Course  Completed

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Degree 【 display / non-display 】

  • The Graduate University for Advanced Studies -  Doctor (Science)

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Campus Career 【 display / non-display 】

  • 2022.01
    -
    Now

    Akita University   Graduate School of Medicine   Doctorial Course in Medicine   Organ Function-Oriented Medicine   Department of Integrative Physiology   Assistant Professor  

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External Career 【 display / non-display 】

  • 2014.08
    -
    2015.03

    National Institutes of Natural Sciences   Researcher  

  • 2011.04
    -
    2014.07

    National Institutes of Natural Sciences  

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Research Areas 【 display / non-display 】

  • Life Science / Physiology

  • Life Science / Clinical pharmacy

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Research Achievements 【 display / non-display 】

    ◆Original paper【 display / non-display 】

  • Cardioprotective effects of Moku-boi-to and its impact on AngII-induced cardiomyocyte hypertrophy.

    Hideaki Tagashira, Fumiha Abe, Kaori Sato-Numata, Karen Aizawa, Kei Hirasawa, Yoshinobu Kure, Daiki Iwata, Tomohiro Numata

    Frontiers in cell and developmental biology   11   1264076 - 1264076   2023.11  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • 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   2023.09  [Refereed]

    Research paper (journal)   International Co-author

    DOI

  • Intermediate conductance Ca2+ -activated potassium channels are activated by functional coupling with stretch-activated nonselective cation channels in cricket myocytes

    Tomohiro Numata, Kaori Sato-Numata, Masami Yoshino

    Frontiers in Insect Science     2023.01  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • TRPM7 is an essential regulator for volume-sensitive outwardly rectifying anion channel

    Tomohiro Numata, Kaori Sato-Numata, Meredith C. Hermosura, Yasuo Mori, Yasunobu Okada

    Communications Biology ( Springer Science and Business Media LLC )  4 ( 1 ) 599 - 599   2021.12  [Refereed]

    Research paper (journal)   International Co-author

    <title>Abstract</title>Animal cells can regulate their volume after swelling by the regulatory volume decrease (RVD) mechanism. In epithelial cells, RVD is attained through KCl release mediated via volume-sensitive outwardly rectifying Cl<sup>−</sup> channels (VSOR) and Ca<sup>2+</sup>-activated K<sup>+</sup> channels. Swelling-induced activation of TRPM7 cation channels leads to Ca<sup>2+</sup> influx, thereby stimulating the K<sup>+</sup> channels. Here, we examined whether TRPM7 plays any role in VSOR activation. When TRPM7 was knocked down in human HeLa cells or knocked out in chicken DT40 cells, not only TRPM7 activity and RVD efficacy but also VSOR activity were suppressed. Heterologous expression of TRPM7 in TRPM7-deficient DT40 cells rescued both VSOR activity and RVD, accompanied by an increase in the expression of LRRC8A, a core molecule of VSOR. TRPM7 exerts the facilitating action on VSOR activity first by enhancing molecular expression of LRRC8A mRNA through the mediation of steady-state Ca<sup>2+</sup> influx and second by stabilizing the plasmalemmal expression of LRRC8A protein through the interaction between LRRC8A and the <italic>C</italic>-terminal domain of TRPM7. Therefore, TRPM7 functions as an essential regulator of VSOR activity and LRRC8A expression.

    DOI PubMed

  • Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 2: Functional and Molecular Properties of ASOR/PAC Channels and Their Roles in Cell Volume Dysregulation and Acidotoxic Cell Death

    Yasunobu Okada, Kaori Sato-Numata, Ravshan Z. Sabirov, Tomohiro Numata

    Frontiers in Cell and Developmental Biology   9   702317   2021.07  [Refereed]  [Invited]

    Research paper (journal)   International Co-author

    For survival and functions of animal cells, cell volume regulation (CVR) is essential. Major hallmarks of necrotic and apoptotic cell death are persistent cell swelling and shrinkage, and thus they are termed the necrotic volume increase (NVI) and the apoptotic volume decrease (AVD), respectively. A number of ubiquitously expressed anion and cation channels play essential roles not only in CVR but also in cell death induction. This series of review articles address the question how cell death is induced or protected with using ubiquitously expressed ion channels such as swelling-activated anion channels, acid-activated anion channels, and several types of TRP cation channels including TRPM2 and TRPM7. In the Part 1, we described the roles of swelling-activated VSOR/VRAC anion channels. Here, the Part 2 focuses on the roles of the acid-sensitive outwardly rectifying (ASOR) anion channel, also called the proton-activated chloride (PAC) anion channel, which is activated by extracellular protons in a manner sharply dependent on ambient temperature. First, we summarize phenotypical properties, the molecular identity, and the three-dimensional structure of ASOR/PAC. Second, we highlight the unique roles of ASOR/PAC in CVR dysfunction and in the induction of or protection from acidotoxic cell death under acidosis and ischemic conditions.

    DOI

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Grant-in-Aid for Scientific Research 【 display / non-display 】

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2021.04  -  2024.03 

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2021.04  -  2024.03 

  • Grant-in-Aid for JSPS Fellows

    Project Year： 2018.10  -  2022.03 

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2017.04  -  2020.03 

  • Grant-in-Aid for JSPS Fellows

    Project Year： 2015.04  -  2019.03 

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Presentations 【 display / non-display 】

  • LRRC8Dのヒト上皮細胞における調節性容積減少への役割

    佐藤（沼田）かお理, 鈴木太郎, 酒井彩子, 森俊太郎, 岡田泰伸, 沼田朋大

    日本生理学会 第100回記念大会  (国立京都国際会館)  2023.03  -  2023.03  日本生理学会第100回記念大会

  • バソプレシンニューロンは高浸透圧刺激に対して分泌性容積減少（SVD）と調節性容積増加（RVI）という相反性容積応答をする

    佐藤（沼田）かお理，沼田朋大，上田陽一，岡田泰伸

    第126回 日本解剖学会総会・全国学術集会, 第98回 日本生理学会大会  2021.03  -  2021.03 

  • Sensitivity of voltage-dependent Ca2+ channels in rat AVP neurons to an anthranilic acid derivative

    Kaori Sato-Numata，Tomohiro Numata，Yoichi Ueta，Yasunobu Okada

    The 9th Federation of Asian and Oceanian Physiological Societies (FAOPS) Congress  2019.03  -  2019.03 

  • Ionic mechanisms of cell volume regulation under hypo/hyperosmotic conditions in AVP neurons and effects of AVP secretion thereon

     [Invited]

    2018.07  -  2018.07 

  • The role of somatodendritic release of arginine vasopressin in rat vasopressin neurons under hypoosmotic conditions.

     [Invited]

    2012.02  -  2012.02 

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