MATSUOKA Satoshi

FacultyMorphological and Physiological Sciences, Integrative Systems Physiology
Teacher OrganizationMorphological and Physiological Sciences
Education and
 Research Organization
Faculty of Medical Sciences, School of Medicine
PositionProfessor
Last Updated: 19/07/23 20:20

Researcher Profile & Settings

Name

    MATSUOKA Satoshi

Research Areas

  • Medicine,dentistry, and pharmacy / Basic medicine Collaboration in Organization
  • Medicine,dentistry, and pharmacy / Basic medicinemathematical biology, computational physiology /  Collaboration in Organization
  • Medicine,dentistry, and pharmacy / Basic medicine / Physiology of mitochondriaMitochondria, Transporters, Channels, Cell /  Collaboration in Organization

Affiliation

  •  Morphological and Physiological Sciences, Integrative Systems Physiology Professor

Association Memberships

    The Physiological Society member,Physiological Society of Japan councilor,Biophysical Society member,Japanese Circulation Society member,Japanese Society of Electrocardiology member,

Research Activities

Published Papers

  • The ventromedial hypothalamus oxytocin induces locomotor behavior regulated by estrogen.
    Narita K, Murata T, Matsuoka S
    Physiol Behav 164(16) 107-112 May  2016 Refereed
  • Roles of the mitochondrial Na+-Ca2+ exchanger, NCLX, in B lymphocyte chemotaxis.
    Kim B, Takeuchi A, Hikida M, Matsuoka S
    Sci Rep 22(6) 28378-28378 Jun.  2016 Refereed
  • Dysregulation of a potassium channel, THIK-1, targeted by caspase-8 accelerates cell shrinkage.
    Sakamaki K, Ishii TM, Sakata T, Takemoto K, Takagi C, Takeuchi A, Morishita R, Takahashi H, Nozawa A, Shinoda H, Chiba K, Sugimoto H, Saito A, Tamate S, Satou Y, Jung SK, Matsuoka S, Koyamada K, Sawasaki T, Nagai T, Ueno N.
    Biochim Biophys Acta 1863(11) 2766-2783 Nov.  2016 Refereed
  • A simulation study on the constancy of cardiac energy metabolites during workload transition.
    Saito R, Takeuchi A, Himeno Y, Inagaki N, Matsuoka S
    J Physiol 594(23) 6929-6945 Dec.  2016 Refereed
  • The destiny of Ca2+ released by mitochondria
    Takeuchi A, Kim B, Matsuoka S
     65(1) 42332 Jan.  2015 Refereed
  • Tracking and quantification of dendritic cell migration and antigen trafficking between the skin and lymph nodes
    Tomura M, Hata A, 松岡 達, Shand FH, Nakanishi Y, Ikebuchi R, Ueha S, Tsutsui H, Inaba K, Matsushima K, Miyawaki A, Kabashima K, Watanabe T, Kanagawa O
    Sci Rep. 4 6030 Aug.  2014 Refereed
  • Identification of chemicals inducing cardiomyocyte proliferation in developmental stage-specific manner with pluripotent stem cells
    Uosaki H, Magadum A, Seo K, Fukushima H, Takeuchi A, Nakagawa Y, Moyes KW, Narazaki G, Kuwahara K, Laflamme M, Matsuoka S, Nakatsuji N, Nakao K, Kwon C, Kass DA, Engel FB, Yamashita JK
    Circulation-Cardiovascular Genetics 6(6) 624-33 Dec.  2013 Refereed
  • The mitochondrial Na+-Ca2+ exchanger, NCLX, regulates automaticity of HL-1 cardiomyocytes
    Takeuchi A, Kim B, Matsuoka S
    Scientific Reports 3 2766 Sep.  2013 Refereed
  • Basophils are required for the induction of Th2 immunity to haptens and peptide antigens
    Otsuka A, Nakajima S, Kubo M, Egawa G, Honda T, Kitoh A, Nomura T, Hanakawa S, Sagita Moniaga C, Kim B, Matsuoka S, Watanabe T, Miyachi Y, Kabashima K
    Nature Communications 4 1738 Apr.  2013 Refereed
  • Mitochondria Na+-Ca2+ exchange in cardiomyocytes and lymphocytes
    Kim B, Takeuchi A, Koga O, Hikida M, Matsuoka S
    Advances in Experimental Medicine and Biology 961 193-201. 2013 Refereed
  • NHE-1 blockade reversed changes in calcium transient in myocardial slices from isoproterenol-induced hypertrophied rat left ventricle
    Hattori H, Takeshita D, Takeuchi A, Kim B, Shibata M, Matsuoka S, Obata K, Mitsuyama S, Zhang GX, Takaki M
    Biochemical and Biophysical Research Communications 419(2) 431-5 Mar.  2012 Refereed
  • Pivotal role of mitochondrial Na+-Ca2+ exchange in antigen receptor mediated Ca2+ signalling in DT40 and A20 B lymphocytes
    Kim B, Takeuchi A, Koga O, Hikida M, Matsuoka S
    Journal of Physiology 590(3) 459-74 Feb.  2012 Refereed
  • Impairment of Ubiquitin-Proteasome System by E334K cMyBPC Modifies Channel Proteins, Leading to Electrophysiological Dysfunction
    Bahrudin U, Morikawa K, Takeuchi A, Kurata Y, Miake J, Mizuta E, Adachi K, Higaki K, Yamamoto Y, Shirayoshi Y, Yoshida A, Kato M, Yamamoto K, Nanba E, Morisaki H, Morisaki T, Matsuoka S, Ninomiya H, Hisatome I
    Journal of Molecular Biology 413(4) 857-78 Nov.  2011 Refereed
  • Requirement of Interaction between Mast Cells and Skin Dendritic Cells to Establish Contact Hypersensitivity
    Otsuka A, Kubo M, Honda T, Egawa G, Nakajima S, Tanizaki H, Kim B, Matsuoka S, Watanabe T, Nakae S, Miyachi Y, Kabashima K
    PLoS One 6(9) e25538 Sep.  2011 Refereed
  • Minimum Information about a Cardiac Electrophysiology Experiment (MICEE): Standardised reporting for model reproducibility, interoperability, and data sharing
    Quinn TA, Granite S, Allessie MA, Matsuoka S, Kohl P
    Progress in Biophysics and Molecular Biology 107(1) 4-10. Jan.  2011 Refereed
  • Role of the Mitochondrial Na+-Ca2+Exchanger, NCLX, in the Generation of Cardiac Automaticity
    Takeuchi Ayako;Matsuoka Satoshi
    Japanese Journal of Electrocardiology 34(2) 69-81 2014
    Mitochondria are known as ATP-producing factories as well as Ca2+ stores. Mitochondrial Ca2+ (Ca2+m) changes dynamically, and this change is mainly balanced by an influx via a Ca2+ uniporter (MCU) and an efflux via a Na+-Ca2+ exchanger (NCLX). It has been suggested that Ca2+m is involved in regulating mitochondrial energy metabolism. However, little is known about the roles of NCLX in cardiomyocytes, where repetitive Ca2+ transients occur and where a huge amount of ATP is generated and utilized. To clarify its roles, we carried out a study combining NCLX knockdown in the spontaneously beating atrial myocyte-derived cell line HL-1 and mathematical simulations. NCLX knockdown using siRNA resulted in -50% reduction of its mRNA and protein expressions, attenuating Ca2+m efflux and increasing Ca2+m content. Cycle length of spontaneous Ca2+ oscillation and action potential generation were markedly prolonged. The upstrokes of action potential and Ca2+ transient were slower, and sarcoplasmic reticulum (SR) Ca2+ content and reuptake were reduced by knocking down NCLX. Analysis of a mathematical model of HL-1 demonstrated that a substantial amount of Ca2+ is transferred either directly or indirectly via NCLX from mitochondria to SR and that blocking NCLX reduces the SR Ca2+ content to slow SR Ca2+ leak, which triggers automaticity. We propose that Ca2+m dynamics via NCLX is involved in the generation of abnormal automaticity and arrhythmia.
  • Patient-Specific Human Induced Pluripotent Stem Cell Model Assessed with Electrical Pacing Validates S107 as a Potential Therapeutic Agent for Catecholaminergic Polymorphic Ventricular Tachycardia.
    Sasaki Kenichi;Makiyama Takeru;Yoshida Yoshinori;Wuriyanghai Yimin;Kamakura Tsukasa;Nishiuchi Suguru;Hayano Mamoru;Harita Takeshi;Yamamoto Yuta;Kohjitani Hirohiko;Hirose Sayako;Chen Jiarong;Kawamura Mihoko;Ohno Seiko;Itoh Hideki;Takeuchi Ayako;Matsuoka Satoshi;Miura Masaru;Sumitomo Naokata;Horie Minoru;Yamanaka Shinya;Kimura Takeshi
    PloS one 11(10) 2016 Refereed
    INTRODUCTION:Human induced pluripotent stem cells (hiPSCs) offer a unique opportunity for disease modeling. However, it is not invariably successful to recapitulate the disease phenotype because of the immaturity of hiPSC-derived cardiomyocytes (hiPSC-CMs). The purpose of this study was to establish and analyze iPSC-based model of catecholaminergic polymorphic ventricular tachycardia (CPVT), which is characterized by adrenergically mediated lethal arrhythmias, more precisely using electrical pacing that could promote the development of new pharmacotherapies.;METHOD AND RESULTS:We generated hiPSCs from a 37-year-old CPVT patient and differentiated them into cardiomyocytes. Under spontaneous beating conditions, no significant difference was found in the timing irregularity of spontaneous Ca2+ transients between control- and CPVT-hiPSC-CMs. Using Ca2+ imaging at 1 Hz electrical field stimulation, isoproterenol induced an abnormal diastolic Ca2+ increase more frequently in CPVT- than in control-hiPSC-CMs (control 12% vs. CPVT 43%, p<0.05). Action potential recordings of spontaneous beating hiPSC-CMs revealed no significant difference in the frequency of delayed afterdepolarizations (DADs) between control and CPVT cells. After isoproterenol application with pacing at 1 Hz, 87.5% of CPVT-hiPSC-CMs developed DADs, compared to 30% of control-hiPSC-CMs (p<0.05). Pre-incubation with 10 μM S107, which stabilizes the closed state of the ryanodine receptor 2, significantly decreased the percentage of CPVT-hiPSC-CMs presenting DADs to 25% (p<0.05).;CONCLUSIONS:We recapitulated the electrophysiological features of CPVT-derived hiPSC-CMs using electrical pacing. The development of DADs in the presence of isoproterenol was significantly suppressed by S107. Our model provides a promising platform to study disease mechanisms and screen drugs.
  • Uncovering the arrhythmogenic potential of TRPM4 activation in atrial-derived HL-1 cells using novel recording and numerical approaches
    Hu Y, Duan Y, Takeuchi A, Hai-Kurahara L, Ichikawa J, Hiraishi K, Numata T, Ohara H, Iribe G, Nakaya M, Mori MX, Matsuoka S, Ma G, Inoue R
    Cardiovascular Research 113(10) 1243-1255 Aug.  2017 Refereed

Books etc

  • Patch clamp techniques. From beginning to advanced protocols.
    Matsuoka S, Takeuchi A
     2012
  • プログレッシブ 生命科学
    松岡 達
     Sep.  2014

Conference Activities & Talks

  • Mitochondrial Ca2+ and ROS regulation
    Satoshi Matsuoka
    University of California-Davis Cardiovascular Symposium, Mechanics and Energetics in Cardiac Arrhythmias and Heart Failure Feb.  2018 University of California-Davis
  • Na/Ca exchange and Mitochondria function. The use of Mathematical models.
    Satoshi Matsuoka
    38th world congress of the International Union of Physiological Sciences Aug.  2017 International Union of Physiological Sciences
  • Frequency-dependences of action potential and Ca2+ transient and roles of mitochondrial Na+/Ca2+ exchange in mice ventricular myocytes
    Yukari Takeda, Misaki Tsukioka, Shino Fujisawa, Moe Fujisawa, Yousuke Shimizu, Erika Iwai, Rena Horie, Saki Matsunaka, Ayako Takeuchi and Satoshi Matsuoka
    2017 Cardiac Physiome Workshop Nov.  2017 Cardiac Physiome Society
  • Dysregulation of a potassium channel, THIK-1, targeted by the caspase accelerates cell shrinkage during apoptosis
    Kazuhiro Sakamaki, Toshiya Sakata, Ayako Takeuchi, Chiyo Takagi, Hajime Shinoda, Akiko Saito, Takeharu Nagai, Satoshi Matsuoka, Naoto Ueno
     Dec.  2017 The Molecular Biology Society of Japan
  • Intracellular localization of mitochondrial Na+-Ca2+ exchanger NCLX in mice ventricular myocytes
    Ayako Takeuchi, Satoshi Matsuoka
    62nd Biophysical Meeting Feb.  2018 Biophysical Society
  • ミトコンドリア-小胞体Ca2+クロストークに関するフィジオーム研究
    竹内綾子, 松岡達
    日本膜学会第38年会 May  2016
  • 新規ミトコンドリアエネルギー代謝数理モデルを用いた心臓エネルギー代謝制御メカニズムの解析
    竹内綾子、齋藤隆太、姫野友紀子、松岡達
    平成28年度生理学研究所 研究会「心臓・血管系の包括的な機能統合研究」 Oct.  2016
  • 神経膠芽腫細胞遊走におけるミトコンドリア動態のシングルファイバーを用いた解析
    河合 佑介, 竹内 綾子, 藤田 聡, 松岡 達
    第63回 中部日本生理学会 Nov.  2016
  • 心臓仕事量増大時におけるエネルギー代謝産物安定性制御メカニズムに関する数理解析
    竹内綾子、齋藤隆太、姫野友紀子、松岡達
    第63回 中部日本生理学会 Nov.  2016
  • A simulation study on roles of Ca2+ in constancy of cardiac energy metabolites during workload transition.
    Ayako Takeuchi, Ryuta Saito, Yukiko Himeno, Satoshi Matsuoka.
    2016 Cardiac Physiome Workshop Aug.  2016
  • A theoretical study on the roles of Ca2+ in the energy metabolite stability during cardiac workload transition.
    Ayako Takeuchi, Ryuta Saito, Yukiko Himeno. Satoshi Matsuoka.
    Biophysical Society 61th Annual Meeting Feb.  2017
  • Involvement of vitamin D receptor and its related genes in the generation of rhythmic Ca transient in murine atrial myocyte-derived cell line HL-1.
    Takuya Murata, Ayako Takeuchi, Satoshi Matsuoka.
    The 94th Annual Meeting of the Physiological Society of Japan Mar.  2017
  • Mechanisms for external K+ dependence of K+ permeation and gating of Kir2.1 inward rectifier K+ channel
    Keiko Ishihara, Satoshi Matsuoka, Makoto Takano
    The 94th Annual Meeting of the Physiological Society of Japan Mar.  2017
  • Physiome study on the roles of mitochondria-endoplasmic reticulum Ca2+ crosstalk in lymphocytes.
    Ayako Takeuchi, Bongju Kim, Satoshi Matsuoka.
    The 94th Annual Meeting of the Physiological Society of Japan Mar.  2017
  • A simulation study on Ca2+ regulation of energy metabolism in cardiac mitochondria.
    Satoshi Matsuoka, Ayako Takeuchi, Ryuta Saito, Yukiko Himeno.
    The 94th Annual Meeting of the Physiological Society of Japan Mar.  2017
  • Contribution of mitochondria to the generation of automaticity of sinoatrial node cells; a simulation study
    Takeuchi A, Horiguchi K, Iino S, Fukazawa Y, Matsuoka S
    e-Heartシンポジウム Sep.  2015
  • 心筋細胞 HL -1の周期的 Ca transient発生におけるvitamin D receptorの関与
    村田 拓也、竹内 綾子、松岡 達
    生理学研究所研究会 2015「心臓・血管系の包括的な機能統合研究」 Oct.  2015
  • Simulation analysis of automaticity of sinoatrial node
    Ayako Takeuchi, Satoshi Matsuoka
    Society for Mathematical Biology 2015 conference Jul.  2015
  • Physiome study on mitochondrial Ca2+ dynamics.
    Satoshi Matsuoka and Ayako Takeuchi
    67th Annual meeting of the Korean Physiological Society Oct.  2015
  • 心臓リズム・代謝制御機構
    松岡 達
    第93回日本生理学会大会 Mar.  2016
  • Involvement of vitamin D receptor in the generation of rhythmic Ca transient in murine atrial myocyte-derived cell line HL-1.
    Murata Takuya, Takeuchi Ayako, Matsuoka Satoshi.
    The 93 Annual Meeting of the Physiological Society of Japan Mar.  2016
  • Construction of a mathematical model of mouse sinoatrial node cell considering structural crosstalk between mitochondria and sarcoplasmic reticulum.
    Ayako Takeuchi, Satoshi Matsuoka.
    The 93 Annual Meeting of the Physiological Society of Japan Mar.  2016
  • Beta-adrenergic stimulation induced cardiac fibrosis in Tric-A-knockout mice.
    Daiju Yamazaki, Ayako Takeuchi, Chengzhu Zhao, Miyuki Nishi, Satoshi Matsuoka, Hiroshi Takeshima.
    The 93 Annual Meeting of the Physiological Society of Japan Mar.  2016
  • Numerical model-based investigation of TRPM4 channel in cardiac remodeling-ssociated arrhythmogenicity
    Ryuji Inoue, Yaopeng Hu, Yubin Duan, Ayako Takeuchi, Lin Hai Kurahara-hai, Jun Ichikawa, Satoshi Matsuoka.
    The 93 Annual Meeting of the Physiological Society of Japan Mar.  2016
  • リンパ球細胞走化・遊走におけるイオン・水動態
    Takeuchi A, Matsuoka S, Kim B
     Mar.  2015
  • Crosstalk between mitochondria and sarcoplasmic reticulum in sinoatrial node cells
    竹内 綾子, 堀口 和秀, 飯野 哲, 深澤 有吾, 松岡 達
     Mar.  2015
  • ミトコンドリアによる心自動能制御メカニズムの多階層解析
    竹内 綾子, 松岡 達
     Mar.  2015
  • HD physiological analysis of mechanisms underlying generation of cardiac automaticity via mitochondria
    Takeuchi A, Matsuoka S
    Grant-in-Aid for Scientific Research on Innovative Area “HD Physiology” The Final HD Physiology Symposium Mar.  2015
  • Rat uterine oxytocin receptor and estrogen receptor a and b mRNA levels are regulated by estrogen through multiple estrogen receptors
    村田 拓也, 市丸 徹, 成田 和巳, 松岡 達
     Mar.  2015
  • 全身麻酔中・集中治療中の新しい循環管理モニタの開発ー血液循環の自動管理を目指してー
    重見 研司, 小畑 友里江, 高久 明子, 松岡 達, 早渕 光代, デイビッド カイェンベ, 濵田 敏彦, 岡藤 和博
     Mar.  2015
  • ミトコンドリアモデル
    Matsuoka S, Takeuchi A
     Feb.  2015
  • 左心室大動脈結合状態(Ees/Ea)と一回拍出量(SV)から左心室拡張末期容量(Ved)を算出する方法
    早渕 光代, 小畑 友里江, 高久 明子, デイビッド カイェンベ, 早渕 由朗, 濵田 敏彦, 松岡 達, 重見 研司
     Dec.  2014
  • 数理解析から解き明かす細胞機能
    松岡 達
     Dec.  2014
  • ラット視床下部腹内側核に投与したオキシトシンにより誘発される走行運動に対するエストロジェンの増強効果
    成田 和巳, 村田拓也, 松岡達
     Nov.  2014
  • ラット子宮オキシトシンレセプターのエストロゲンによる調節
    村田 拓也, 成田 和巳, 市丸 徹, 松岡 達
     Nov.  2014
  • ミトコンドリアNa+-Ca2+交換輸送体NCLX によるB リンパ球細胞走化の調節
    Takeuchi A, Matsuoka S, Kim B
     Nov.  2014
  • 心筋梗塞時の活動電位の変化 ~コンピュータシミュレーションを用いての検討~
    松岡 達
     Aug.  2014
  • Simulation study of Ca2+ response in lymphocytes
    Matsuoka S, Kim B, Takeuchi A, Koga O, Hikida M
    The 91st Annual Meeting of the Physiological Society of Japan Mar.  2014
  • Mitochondrial Na-Ca exchanger NCLX-mediated mitochondria-sarcoplasmic reticulum Ca crosstalk and cardiomyocyte automaticity
    Takeuchi A, Matsuoka S
    The 91st Annual Meeting of the Physiological Society of Japan Mar.  2014
  • 細胞容積調節におけるチャネル・トランスポーターの寄与~包括的心筋細胞数理モデルと細胞生理実験によるイオン・水動態の解明~
    竹内綾子, 松岡達
     Mar.  2014
  • Mitochondria-endoplasmic/sarcoplasmic reticulum Ca crosstalk and cellular function
    Takeuchi A, Kim B, Matsuoka S
    The 91st Annual Meeting of the Physiological Society of Japan Mar.  2014
  • システム生理学研究による細胞内イオンダイナミクス―細胞生理機能連関の包括的理解
    竹内綾子, 松岡達
     Nov.  2013
  • 洞房結節細胞自動能におけるミトコンドリアNCLXの寄与―シミュレーション解析
    竹内綾子, 松岡達
     Nov.  2013
  • Contribution of mitochondrial Na+-Ca2+ exchanger, NCLX, in making the cardiac rhythmicity
    Takeuchi A, Kim B, Matsuoka S
    The 2nd HD Physiology International Symposium: Multi-Level Systems Biology May  2013
  • Theoretical analysis of mitochondrial NCX-mediated regulation of automaticity in sinoatrial node cells
    Takeuchi A, Kim B, Matsuoka S
    The 2nd HD Physiology International Symposium: Multi-Level Systems Biology May  2013
  • Simulation analyses of the role of NCLX, a mitochondrial Na+-Ca2+ exchanger, on the regulation of automaticity in sinoatrial node cells
    Takeuchi A, Matsuoka S
    2013 Cardiac Physiome Workshop Jan.  2013
  • Mitochondria-sarcoplasmic reticulum Ca2+ communication on the rhythmicity of sinoatrial node cells
    Matsuoka S, Takeuchi A
    2013 Cardiac Physiome Workshop Jan.  2013
  • Mitochondrial NCX controls directional migration of B lymphocytes
    Kim B, Takeuchi A, Matsuoka S
    The 90th Annual Meeting of the Physiological Society of Japan Mar.  2013
  • Theoretical analysis of mitochondrial NCX (NCLX)-mediated regulation of cardiac automaticity
    Takeuchi A, Kim B, Matsuoka S
    The 90th Annual Meeting of the Physiological Society of Japan Mar.  2013
  • Role of mitochondrial NCX on CXCL12-induced chemotaxis in A20 B lymphocytes
    Kim B, Matsuoka S, Takeuchi A
    57th Annual Meeting of Biophysical Society Feb.  2013
  • Prolongation of beating rate caused by reduction of NCLX, a mitochondrial Na+-Ca2+ exchanger, in HL-1 cardiomyocytes.
    松岡 達, Kim B, Takeuchi A
    57th Annual Meeting of Biophysical Society Feb.  2013