SATO-NUMATA Kaori

写真a

Affiliation

Graduate School of Medicine  Doctorial Course in Medicine  Organ Function-Oriented Medicine  Department of Integrative Physiology

Research Interests 【 display / non-display 】

  • 浸透圧センサー

  • イオンチャネル

  • カチオンチャネル

  • 漢方薬

  • cell physiology

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Graduating School 【 display / non-display 】

  • 2002.04
    -
    2006.03

    Tokyo Gakugei University     Graduated

Graduate School 【 display / non-display 】

  • 2006.04
    -
    2011.03

    The Graduate University for Advanced Studies    Doctor's Course  Completed

Degree 【 display / non-display 】

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

Campus Career 【 display / non-display 】

  • 2026.06
    -
    Now

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

  • 2022.01
    -
    2026.05

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

External Career 【 display / non-display 】

  • 2026.06
     
     

    Akita University   Lecturer  

  • 2024.12
     
     

    Akita University   Graduate School of Medicine Doctoral Course in Medicine  

  • 2022.01
    -
    2024.11

    Akita University   Graduate School of Medicine Doctoral Course in Medicine   Assistant Professor  

  • 2014.08
    -
    2015.03

    National Institutes of Natural Sciences   Researcher  

  • 2011.04
    -
    2014.07

    National Institutes of Natural Sciences  

Research Areas 【 display / non-display 】

  • Life Science / Physiology

  • Life Science / Clinical pharmacy

  • Life Science / Gastroenterology

  • Life Science / Metabolism and endocrinology

 

Research Achievements 【 display / non-display 】

    ◆Original paper【 display / non-display 】

  • Association between Go-rei-san administration and blood pressure reduction in neurosurgical inpatients: A retrospective observational study with complementary analyses of AQP4 function

    Fumiha Abe, Ryo Takayama, Kaori Sato-Numata, Ayako Sakai, Hajime Nakae, Yumiko Akamine, Tomohiro Numata

    European Journal of Integrative Medicine ( European Journal of Integrative Medicine )  87 ( 102751 )   2026.10  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • Hange-Shashin-to Suppresses Serotonin-Induced Neurogenic Intestinal Contraction via Inhibition of 5-HT3A Receptor Signaling

    Kaori Sato-Numata, Ryo Takayama, Ayako Sakai, Tomohiro Numata

    Cellular physiology and biochemistry   60 ( 4 ) 427 - 444   2026.08  [Refereed]

    Research paper (journal)   Domestic Co-author

    BACKGROUND/AIMS: Hange-shashin-to (HST) is a standardized multi-component herbal formulation widely used for the treatment of irritable bowel syndrome (IBS), a functional gastrointestinal disorder characterized by dysregulated serotonergic signaling and abnormal intestinal motility. Despite its clinical application, the cellular mechanisms underlying its therapeutic effects remain unclear. This study investigated the effects of HST on serotonin (5-HT)-induced neuronal responses and the underlying role of 5-HT3A receptor signaling. MATERIALS: Differentiated PC12 cells were used as a neuron-like model to evaluate 5-HT-induced cell shrinkage, membrane depolarization, intracellular Ca²⁺ elevation, and acetylcholine release. Whole-cell patch-clamp recordings were performed in HEK293T cells expressing 5-HT3A receptors to examine receptor-mediated cation currents. The effects of HST on 5-HT-induced colonic contractions were further evaluated using ex vivo rat colonic tissue. RESULTS: HST attenuated 5-HT-induced cell shrinkage in a concentration-dependent manner and suppressed membrane depolarization, intracellular Ca²⁺ elevation, and acetylcholine release in PC12 cells. Patch-clamp analysis demonstrated that HST directly inhibited 5-HT3A receptor-mediated cation currents without altering voltage dependence or reversal potential. Furthermore, HST significantly reduced 5-HT-induced colonic contractions, with efficacy comparable to that of the selective 5-HT3 receptor antagonist ramosetron. CONCLUSION: HST suppresses 5-HT-induced neuronal excitation through inhibition of 5-HT3A receptor-mediated ion channel activity, resulting in reduced downstream intestinal motor responses. These findings identify the 5-HT3A receptor as a molecular target of HST and provide mechanistic insight into its pharmacological actions on 5-HT-mediated intestinal dysfunction.

    DOI PubMed

  • Atrial TRPM2 Channel-Mediated Ca2+ Influx Regulates ANP Secretion and Protects Against Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis

    Tomohiro Numata, Hideaki Tagashira, Kaori Sato-Numata, Meredith C Hermosura, Fumiha Abe, Ayako Sakai, Shinichiro Yamamoto, Hiroyuki Watanabe

    Cells ( MDPI )  15 ( 24 )   2025.12  [Refereed]

    Research paper (journal)   Single author

    DOI

  • Role of Piezo2 in Schwann Cell Volume Regulation and its Impact on Neurotrophic Release Regulation

    Chawapun Suttinont, Katsuyuki Maeno, Mamiko Yano, Kaori Sato-Numata, Tomohiro Numata, Moe Tsutsumi

    Cellular Physiology and Biochemistry   58 ( 4 ) 292 - 310   2024.07  [Refereed]

    Research paper (journal)   Single author

    BACKGROUND/AIMS: Tactile perception relies on mechanoreceptors and nerve fibers, including c-fibers, Aβ-fibers and Aδ-fibers. Schwann cells (SCs) play a crucial role in supporting nerve fibers, with non-myelinating SCs enwrapping c-fibers and myelinating SCs ensheathing Aβ and Aδ fibers. Recent research has unveiled new functions for cutaneous sensory SCs, highlighting the involvement of nociceptive SCs in pain perception and Meissner corpuscle SCs in tactile sensation. Furthermore, Piezo2, previously associated with Merkel cell tactile sensitivity, has been identified in SCs. The goal of this study was to investigate the channels implicated in SC mechanosensitivity and the release process of neurotrophic factor secretion. METHODS: Immortalized IFRS1 SCs and human primary SCs generated two distinct subtypes of SCs: undifferentiated and differentiated SCs. Quantitative PCR was employed to evaluate the expression of differentiation markers and mechanosensitive channels, including TRP channels (TRPV4, TRPM7 and TRPA1) and Piezo channels (Piezo1 and Piezo2). To validate the functionality of specific mechanosensitive channels, Ca2+ imaging and electronic cell sizing experiments were conducted under hypotonic conditions, and inhibitors and siRNAs were used. Protein expression was assessed by Western blotting and immunostaining. Additionally, secretome analysis was performed to evaluate the release of neurotrophic factors in response to hypotonic stimulation, with BDNF, a representative trophic factor, quantified using ELISA. RESULTS: Induction of differentiation increased Piezo2 mRNA expression levels both in IFRS1 and in human primary SCs. Both cell types were responsive to hypotonic solutions, with differentiated SCs displaying a more pronounced response. Gd3+ and FM1-43 effectively inhibited hypotonicity-induced Ca2+ transients in differentiated SCs, implicating Piezo2 channels. Conversely, inhibitors of Piezo1 and TRPM7 (Dooku1 and NS8593, respectively) had no discernible impact. Moreover, Piezo2 in differentiated SCs appeared to participate in regulatory volume decreases (RVD) after cell swelling induced by hypotonic stimulation. A Piezo2 deficiency correlated with reduced RVD and prolonged cell swelling, leading to heightened release of the neurotrophic factor BDNF by upregulating the function of endogenously expressed Ca2+-permeable TRPV4. CONCLUSION: Our study unveils the mechanosensitivity of SCs and implicates Piezo2 channels in the release of neurotrophic factors from SCs. These results suggest that Piezo2 may contribute to RVD, thereby maintaining cellular homeostasis, and may also serve as a negative regulator of neurotrophic factor release. These findings underscore the need for further investigation into the role of Piezo2 in SC function and neurotrophic regulation.

    DOI PubMed

  • 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

    Cardiomyocyte hypertrophy, induced by elevated levels of angiotensin II (AngII), plays a crucial role in cardiovascular diseases. Current therapeutic approaches aim to regress cardiac hypertrophy but have limited efficacy. Widely used Japanese Kampo medicines are highly safe and potential therapeutic agents. This study aims to explore the impact and mechanisms by which Moku-boi-to (MBT), a Japanese Kampo medicine, exerts its potential cardioprotective benefits against AngII-induced cardiomyocyte hypertrophy, bridging the knowledge gap and contributing to the development of novel therapeutic strategies. By evaluating the effects of six Japanese Kampo medicines with known cardiovascular efficiency on AngII-induced cardiomyocyte hypertrophy and cell death, we identified MBT as a promising candidate. MBT exhibited preventive effects against AngII-induced cardiomyocyte hypertrophy, cell death and demonstrated improvements in intracellular Ca2+ signaling regulation, ROS production, and mitochondrial function. Unexpectedly, experiments combining MBT with the AT1 receptor antagonist losartan suggested that MBT may target the AT1 receptor. In an isoproterenol-induced heart failure mouse model, MBT treatment demonstrated significant effects on cardiac function and hypertrophy. These findings highlight the cardioprotective potential of MBT through AT1 receptor-mediated mechanisms, offering valuable insights into its efficacy in alleviating AngII-induced dysfunction in cardiomyocytes. The study suggests that MBT holds promise as a safe and effective prophylactic agent for cardiac hypertrophy, providing a deeper understanding of its mechanisms for cardioprotection against AngII-induced dysfunction.

    DOI PubMed

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    ◆Other【 display / non-display 】

  • Comprehensive clinical laboratory analysis of the Japanese Kampo medicine “Gorei-san′′ reveals a potential antihypertensive effect supported by aquaporin-related mechanisms

    日本薬学会年会要旨集(Web)   146th   2026

    J-GLOBAL

  • The Role of LRRC8A in Boi-Ogi-To (BOT)-Induced Cellular Fluid Excretion via Volume-Sensitive Outwardly Rectifying Chloride Channels

    佐藤(沼田)かお理, 森俊太郎, 加藤正太郎, 鈴木太郎, 齊藤遥菜, 酒井彩子, 岡田泰伸, 岡田泰伸, 岡田泰伸, 沼田朋大

    日本解剖学会総会・全国学術集会抄録集(CD-ROM)   130th   2025

    J-GLOBAL

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 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 Scientific Research(C)

    Project Year: 2021.04  -  2024.03 

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Presentations 【 display / non-display 】

  • Differences in functional properties between acid-sensitive chloride channels and volume-sensitive chloride channels

    Kaori Sato-Numata  [Invited]

    ICMS (Ion Channel Modulation Symposium) 2024 Japan  (東京大学 弥生講堂 一条ホール)  2024.05  -  2024.05  ソフィオン バイオサイエンス株式会社

  • 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 

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Academic Activity 【 display / non-display 】

  • 2024.04
    -
    Now