2021/12/13 更新

写真a

カタノサカ ユキ
片野坂 友紀
KATANOSAKA Yuki
所属
医歯薬学域 講師
職名
講師

学位

  • 博士(理学) ( 1999年3月   大阪大学 )

研究キーワード

  • calcium signal

  • メカニカルフィードバック

  • ノックアウトマウス

  • メカノセンサー

  • ストレッチ

  • メカニカルストレス

  • メカノバイオロジー

  • メカノトランスダクション

  • TRPV2

研究分野

  • ライフサイエンス / 生理学

  • ライフサイエンス / 医療薬学

  • ライフサイエンス / 医用システム

  • ライフサイエンス / 生物物理学

学歴

  • 大阪大学    

    - 1999年3月

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経歴

  • 岡山大学医歯薬学総合研究科 システム生理   講師

    2019年11月 - 現在

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  • 岡山大学医歯薬学総合研究科   システム生理   助教

    2006年4月 - 2019年10月

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  • 国立循環器病センター研究所   日本学術振興会特別研究員 SPD

    2003年4月 - 2006年3月

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  • 国立循環器病センター研究所   科学技術特別研究員   日本学術振興会特別研究員 PD

    2000年4月 - 2003年3月

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  • 国立循環器病センター研究所   流動研究員

    1999年4月 - 2000年3月

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所属学協会

委員歴

  • 基礎・社会医学系教育企画委員会委員  

    2019年4月 - 現在   

  • 自然生命科学研究支援センター動物資源部門 鹿田施設利用協議会委員  

    2007年4月 - 現在   

  • 医歯薬安全衛生委員会委員  

    2007年4月 - 現在   

 

論文

  • Reduced plasticity and microtubule densification in muscular dystrophy-related cardiomyopathy 招待

    Yuki Katanosaka

    J Gen Physiol   154 ( 9 )   e2021esc45   2022年9月

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    担当区分:筆頭著者, 最終著者, 責任著者  

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  • Involvement of Transient Receptor Potential Vanilloid Channel 2 in the Induction of Lubricin and Suppression of Ectopic Endochondral Ossification in Mouse Articular Cartilage. 査読 国際誌

    Hideki Nakamoto, Yuki Katanosaka, Ryota Chijimatsu, Daisuke Mori, Fengjun Xuan, Fumiko Yano, Yasunori Omata, Yuji Maenohara, Yasutaka Murahashi, Kohei Kawaguchi, Ryota Yamagami, Hiroshi Inui, Shuji Taketomi, Yuki Taniguchi, Motoi Kanagawa, Keiji Naruse, Sakae Tanaka, Taku Saito

    Arthritis & rheumatology (Hoboken, N.J.)   73 ( 8 )   1441 - 1450   2021年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    OBJECTIVE: Transient receptor potential vanilloid channel 2 (TRPV2) is a Ca2+ -permeable channel and plays a role in mediating intracellular Ca2+ current via mechanical stimuli. This study was undertaken to examine the expression and role of TRPV2 in adult articular cartilage and the development of osteoarthritis (OA). METHODS: We examined TRPV2 expression in mouse and human articular cartilage. We analyzed the development of OA in Col2a1-CreERt2 ;Trpv2fl/fl mice and Trpv2fl/fl littermates in the resection of the medial meniscus and medial collateral ligament model (n = 5 each), the destabilization of the medial meniscus model (n = 5 each), and the aging mouse model (n = 8-9 each). We examined marker protein expression in these joints, Ca2+ influx by mechanical stimuli, and downstream pathways in vitro. RESULTS: TRPV2 was expressed in mouse and human articular cartilage and ectopic ossification lesions. In all mouse models of OA examined, Col2a1-CreERt2 ;Trpv2fl/fl mice were observed to have enhanced degradation of articular cartilage accompanied by decreased expression of lubricin/Prg4, and marked formation of periarticular ectopic ossification. Mechanical stress-induced Ca2+ influx was decreased by Trpv2 knockout (KO). Prg4 induction by fluid-flow shear stress was diminished in Trpv2-KO mouse chondrocytes, and this was mediated by the Ca2+ /calmodulin-dependent protein kinase kinase-cyclic AMP response element binding protein axis. Hypertrophic differentiation was enhanced in Trpv2-KO mouse chondrocytes. Increased activity of calcineurin and nuclear translocation of nuclear factor in activated T cells 1 induced by fluid-flow shear stress or TRP agonist treatment was reversed by Trpv2 knockout. CONCLUSION: Our findings demonstrate regulation of articular cartilage by TRPV2 through Prg4 induction and suppression of ectopic ossification.

    DOI: 10.1002/art.41684

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  • Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure. 査読 国際誌

    Yoshihiro Ujihara, Motoi Kanagawa, Satoshi Mohri, Satomi Takatsu, Kazuhiro Kobayashi, Tatsushi Toda, Keiji Naruse, Yuki Katanosaka

    Nature communications   10 ( 1 )   5754 - 5754   2019年12月

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    担当区分:最終著者, 責任著者   記述言語:英語  

    Heart failure is the major cause of death for muscular dystrophy patients, however, the molecular pathomechanism remains unknown. Here, we show the detailed molecular pathogenesis of muscular dystrophy-associated cardiomyopathy in mice lacking the fukutin gene (Fktn), the causative gene for Fukuyama muscular dystrophy. Although cardiac Fktn elimination markedly reduced α-dystroglycan glycosylation and dystrophin-glycoprotein complex proteins in sarcolemma at all developmental stages, cardiac dysfunction was observed only in later adulthood, suggesting that membrane fragility is not the sole etiology of cardiac dysfunction. During young adulthood, Fktn-deficient mice were vulnerable to pathological hypertrophic stress with downregulation of Akt and the MEF2-histone deacetylase axis. Acute Fktn elimination caused severe cardiac dysfunction and accelerated mortality with myocyte contractile dysfunction and disordered Golgi-microtubule networks, which were ameliorated with colchicine treatment. These data reveal fukutin is crucial for maintaining myocyte physiology to prevent heart failure, and thus, the results may lead to strategies for therapeutic intervention.

    DOI: 10.1038/s41467-019-13623-2

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  • TRPV2 is required for mechanical nociception and the stretch-evoked response of primary sensory neurons. 査読

    Katanosaka K, Takatsu S, Mizumura K, Naruse K, Katanosaka Y

    Scientific reports   8 ( 1 )   16782   2018年11月

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    担当区分:最終著者  

    DOI: 10.1038/s41598-018-35049-4

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  • Effects of induced Na+/Ca2+ exchanger overexpression on the spatial distribution of L-type Ca2+ channels and junctophilin-2 in pressure-overloaded hearts 査読

    Yoshihiro Ujihara, Satoshi Mohri, Yuki Katanosaka

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   480 ( 4 )   564 - 569   2016年11月

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    担当区分:最終著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    The Na+/Ca2+ exchanger 1 (NCX1) is an essential Ca2+ efflux system in cardiomyocytes. Although NCX1 is distributed throughout the sarcolemma, a subpopulation of NCX1 is localized to transverse (T)-tubules. There is growing evidence that T-tubule disorganization is a causal event that shifts the transition from hypertrophy to heart failure (HF). However, the detailed molecular mechanisms have not been clarified. Previously, we showed that induced NCX1 expression in pressure-overloaded hearts attenuates defective excitation-contraction coupling and HF progression. Here, we examined the effects of induced NCX1 overexpression on the spatial distribution of L-type Ca2+ channels (LTCCs) and junctophilin-2 (JP2), a structural protein that connects the T-tubule and sarcoplasmic reticulum membrane, in pressure overloaded hearts. Quantitative analysis showed that the regularity of NCX1 localization was significantly decreased at 8 weeks after transverse aortic constriction (TAC)-surgery; however, T-tubule organization and the regularities of LTCC and JP2 immunofluorescent signals were maintained at this time point. These observations demonstrated that release of NCX1 from the T-tubule area occurred before the onset of T-tubule disorganization and LTCC and JP2 mislocalization. Moreover, induced NCX1 over expression at 8 weeks post-TAC not only recovered NCX1 regularity but also prevented the decrease in LTCC and JP2 regularities at 16 weeks post-TAC. These results suggested that NCX1 may play an important role in the proper spatial distribution of LTCC and JP2 in T-tubules in the context of pressure overloading. (C) 2016 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2016.10.090

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  • Induced NCX1 overexpression attenuates pressure overload-induced pathological cardiac remodeling 査読

    Ujihara Y, Iwasaki K, Takatsu S, Hashimoto K, Naruse K, Mohri S, Katanosaka Y

    Cardiovascular Research   111 ( 4 )   348 - 361   2016年9月

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    担当区分:最終著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1093/cvr/cvw113

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  • Involvement of S1P1 receptor pathway in angiogenic effects of a novel adenosine-like nucleic acid analog COA-Cl in cultured human vascular endothelial cells 査読

    Junsuke Igarashi, Takeshi Hashimoto, Yasuo Kubota, Kazuyo Shoji, Tokumi Maruyama, Norikazu Sakakibara, Yoh Takuwa, Yoshihiro Ujihara, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse, Tetsuo Yamashita, Ryuji Okamoto, Katsuya Hirano, Hiroaki Kosaka, Maki Takata, Ryoji Konishi, Ikuko Tsukamoto

    Pharmacology Research and Perspectives   2 ( 5 )   e00068   2014年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley-Blackwell Publishing Ltd  

    COA-Cl (2Cl-C.OXT-A) is a recently developed adenosine-like nucleic acid analog that promotes angiogenesis via the mitogen-activated protein (MAP) kinases ERK1/2. Endothelial S1P1 receptor plays indispensable roles in developmental angiogenesis. In this study, we examined the functions of S1P1 in COA-Cl-induced angiogenic responses. Antagonists for S1P1, W146, and VPC23019, substantially but still partly inhibited the effects of COA-Cl with regard to ERK1/2 activation and tube formation in cultured human umbilical vein endothelial cells (HUVEC). Antagonists for adenosine A1 receptor and purinergic P2Y1 receptor were without effect. Genetic knockdown of S1P1 with siRNA, but not that of S1P3, attenuated COA-Cl-elicited ERK1/2 responses. The signaling properties of COA-Cl showed significant similarities to those of sphingosine 1-phosphate, an endogenous S1P1 ligand, in that both induced responses sensitive to pertussis toxin (Gα i/o inhibitor), 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester) (BAPTA-AM), (calcium chelator), and PP2 (c-Src tyrosine kinase inhibitor). COA-Cl elevated intracellular Ca2+ concentration and induced tyrosine phosphorylation of p130Cas, a substrate of c-Src, in HUVEC. COA-Cl displaced [3H]S1P in a radioligand-binding competition assay in chem-1 cells overexpressing S1P1. However, COA-Cl activated ERK1/2 in CHO-K1 cells that lack functional S1P1 receptor, suggesting the presence of additional yet-to-be-defined COA-Cl target in these cells. The results thus suggest the major contribution of S1P1 in the angiogenic effects of COA-Cl. However, other mechanism such as that seen in CHO-K1 cells may also be partly involved. Collectively, these findings may lead to refinement of the design of this nucleic acid analog and ultimately to development of small molecule-based therapeutic angiogenesis.

    DOI: 10.1002/prp2.68

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  • Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin-like growth factor 1 and aggravates muscular dystrophy in mice 査読

    Fumiaki Saito, Motoi Kanagawa, Miki Ikeda, Hiroki Hagiwara, Toshihiro Masaki, Hidehiko Ohkuma, Yuki Katanosaka, Teruo Shimizu, Masahiro Sonoo, Tatsushi Toda, Kiichiro Matsumura

    HUMAN MOLECULAR GENETICS   23 ( 17 )   4543 - 4558   2014年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Several types of muscular dystrophy are caused by defective linkage between alpha-dystroglycan (alpha-DG) and laminin. Among these, dystroglycanopathy, including Fukuyama-type congenital muscular dystrophy (FCMD), results from abnormal glycosylation of alpha-DG. Recent studies have shown that like-acetylglucosaminyltransferase(LARGE) strongly enhances the laminin-binding activity of alpha-DG. Therefore, restoration of the alpha-DG-laminin linkage by LARGE is considered one of the most promising possible therapies for muscular dystrophy. In this study, we generated transgenic mice that overexpress LARGE (LARGE Tg) and crossed them with dy(2J) mice and fukutin conditional knockout mice, a model for laminin alpha 2-deficient congenital muscular dystrophy (MDC1A) and FCMD, respectively. Remarkably, in both the strains, the transgenic overexpression of LARGE resulted in an aggravation of muscular dystrophy. Using morphometric analyses, we found that the deterioration of muscle pathology was caused by suppression of muscle regeneration. Overexpression of LARGE in C2C12 cells further demonstrated defects in myotube formation. Interestingly, a decreased expression of insulin-like growth factor 1 (IGF-1) was identified in both LARGE Tg mice and LARGE-overexpressing C2C12 myotubes. Supplementing the C2C12 cells with IGF-1 restored the defective myotube formation. Taken together, our findings indicate that the overexpression of LARGE aggravates muscular dystrophy by suppressing the muscle regeneration and this adverse effect is mediated via reduced expression of IGF-1.

    DOI: 10.1093/hmg/ddu168

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  • The significant role of Na<sup>+</sup>/Ca<sup>2+</sup> exchanger 1 on local Ca<sup>2+</sup> control beneath T-tubule membrane 査読

    Yoshihiro Ujihara, Keiichiro Iwasaki, Satomi Takatsu, Ken Hashimoto, Keiji Naruse, Satoshi Mohri, Yuki Katanosaka

    Transactions of Japanese Society for Medical and Biological Engineering   52   212 - O-213   2014年8月

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    担当区分:最終著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Japan Soc. of Med. Electronics and Biol. Engineering  

    Na+/Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    exchanger (NCX1) is essential Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    regulator of myocyte Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    homeostasis and specially localized at transverse tubules (T-tubules) membrane. T-tubules are invaginations of the sarcolemma and critical for myocyte contraction, especially as the main site of excitation-contraction coupling. Therefore, T-tubule disorganization is linked to decreased contractility in heart failure, but the molecular mechanism is not clear. We analyzed the alteration of T-tubule structure and Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    handling during the progression of heart failure after transverse aortic constriction (TAC)-surgery, using cardiac-specific and inducible NCX1 transgenic mice. In progression of cardiac dysfunction, sarcoplasmic reticulum Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    ATPase and NCX1 activity were down-regulated before T-tubule disorganization. The inducing NCX1 overexpression after TAC-surgery prevented T-tubule disorganization and contractile dysfunction under prolonged pressure-overload, with improvement of myocyte Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    handling. These results suggest that local Ca&lt
    inf&gt
    2+&lt
    /inf&gt
    control beneath the T-tubule membrane is crucial for the maintenance of myocyte structure and function, in which NCX1 has a pivotal role.

    DOI: 10.11239/jsmbe.52.O-212

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  • TRPV2 is critical for the maintenance of cardiac structure and function in mice 査読

    Yuki Katanosaka, Keiichiro Iwasaki, Yoshihiro Ujihara, Satomi Takatsu, Koki Nishitsuji, Motoi Kanagawa, Atsushi Sudo, Tatsushi Toda, Kimiaki Katanosaka, Satoshi Mohri, Keiji Naruse

    NATURE COMMUNICATIONS   5   3932   2014年5月

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    担当区分:筆頭著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATURE PUBLISHING GROUP  

    The heart has a dynamic compensatory mechanism for haemodynamic stress. However, the molecular details of how mechanical forces are transduced in the heart are unclear. Here we show that the transient receptor potential, vanilloid family type 2 (TRPV2) cation channel is critical for the maintenance of cardiac structure and function. Within 4 days of eliminating TRPV2 from hearts of the adult mice, cardiac function declines severely, with disorganization of the intercalated discs that support mechanical coupling with neighbouring myocytes and myocardial conduction defects. After 9 days, cell shortening and Ca2+ handling by single myocytes are impaired in TRPV2-deficient hearts. TRPV2-deficient neonatal cardiomyocytes form no intercalated discs and show no extracellular Ca2+-dependent intracellular Ca2+ increase and insulin-like growth factor (IGF-1) secretion in response to stretch stimulation. We further demonstrate that IGF-1 receptor/PI3K/Akt pathway signalling is significantly downregulated in TRPV2-deficient hearts, and that IGF-1 administration partially prevents chamber dilation and impairment in cardiac pump function in these hearts. Our results improve our understanding of the molecular processes underlying the maintenance of cardiac structure and function.

    DOI: 10.1038/ncomms4932

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  • The significant role of Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchanger 1 on local Ca<SUP>2+</SUP> control beneath T-tubule membrane

    Ujihara Yoshihiro, Iwasaki Keiichiro, Takatsu Satomi, Hashimoto Ken, Naruse Keiji, Mohri Satoshi, Katanosaka Yuki

    生体医工学   52   O - 212-O-213   2014年

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    担当区分:最終著者, 責任著者   記述言語:日本語   出版者・発行元:Japanese Society for Medical and Biological Engineering  

    Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchanger (NCX1) is essential Ca<SUP>2+</SUP> regulator of myocyte Ca<SUP>2+</SUP> homeostasis and specially localized at transverse tubules (T-tubules) membrane. T-tubules are invaginations of the sarcolemma and critical for myocyte contraction, especially as the main site of excitation-contraction coupling. Therefore, T-tubule disorganization is linked to decreased contractility in heart failure, but the molecular mechanism is not clear. We analyzed the alteration of T-tubule structure and Ca2+ handling during the progression of heart failure after transverse aortic constriction (TAC)-surgery, using cardiac-specific and inducible NCX1 transgenic mice. In progression of cardiac dysfunction, sarcoplasmic reticulum Ca<SUP>2+</SUP> ATPase and NCX1 activity were down-regulated before T-tubule disorganization. The inducing NCX1 overexpression after TAC-surgery prevented T-tubule disorganization and contractile dysfunction under prolonged pressure-overload, with improvement of myocyte Ca<SUP>2+</SUP> handling. These results suggest that local Ca<SUP>2+</SUP> control beneath the T-tubule membrane is crucial for the maintenance of myocyte structure and function, in which NCX1 has a pivotal role.

    DOI: 10.11239/jsmbe.52.O-212

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  • Impaired viability of muscle precursor cells in muscular dystrophy with glycosylation defects and amelioration of its severe phenotype by limited gene expression 査読

    Motoi Kanagawa, Chih-Chieh Yu, Chiyomi Ito, So-ichiro Fukada, Masako Hozoji-Inada, Tomoko Chiyo, Atsushi Kuga, Megumi Matsuo, Kanoko Sato, Masahiko Yamaguchi, Takahito Ito, Yoshihisa Ohtsuka, Yuki Katanosaka, Yuko Miyagoe-Suzuki, Keiji Naruse, Kazuhiro Kobayashi, Takashi Okada, Shin'ichi Takeda, Tatsushi Toda

    HUMAN MOLECULAR GENETICS   22 ( 15 )   3003 - 3015   2013年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    A group of muscular dystrophies, dystroglycanopathy is caused by abnormalities in post-translational modifications of dystroglycan (DG). To understand better the pathophysiological roles of DG modification and to establish effective clinical treatment for dystroglycanopathy, we here generated two distinct conditional knock-out (cKO) mice for fukutin, the first dystroglycanopathy gene identified for Fukuyama congenital muscular dystrophy. The first dystroglycanopathy modelumyofiber-selective fukutin-cKO [muscle creatine kinase (MCK)-fukutin-cKO] miceushowed mild muscular dystrophy. Forced exercise experiments in presymptomatic MCK-fukutin-cKO mice revealed that myofiber membrane fragility triggered disease manifestation. The second dystroglycanopathy modelumuscle precursor cell (MPC)-selective cKO (Myf5-fukutin-cKO) miceuexhibited more severe phenotypes of muscular dystrophy. Using an isolated MPC culture system, we demonstrated, for the first time, that defects in the fukutin-dependent modification of DG lead to impairment of MPC proliferation, differentiation and muscle regeneration. These results suggest that impaired MPC viability contributes to the pathology of dystroglycanopathy. Since our data suggested that frequent cycles of myofiber degeneration/regeneration accelerate substantial and/or functional loss of MPC, we expected that protection from disease-triggering myofiber degeneration provides therapeutic effects even in mouse models with MPC defects; therefore, we restored fukutin expression in myofibers. Adeno-associated virus (AAV)-mediated rescue of fukutin expression that was limited in myofibers successfully ameliorated the severe pathology even after disease progression. In addition, compared with other gene therapy studies, considerably low AAV titers were associated with therapeutic effects. Together, our findings indicated that fukutin-deficient dystroglycanopathy is a regeneration-defective disorder, and gene therapy is a feasible treatment for the wide range of dystroglycanopathy even after disease progression.

    DOI: 10.1093/hmg/ddt157

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  • Mechanical Stretch Increases the Proliferation While Inhibiting the Osteogenic Differentiation in Dental Pulp Stem Cells 査読

    Masaki Hata, Keiko Naruse, Shogo Ozawa, Yasuko Kobayashi, Nobuhisa Nakamura, Norinaga Kojima, Maiko Omi, Yuki Katanosaka, Toru Nishikawa, Keiji Naruse, Yoshinobu Tanaka, Tatsuaki Matsubara

    TISSUE ENGINEERING PART A   19 ( 5-6 )   625 - 633   2013年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MARY ANN LIEBERT INC  

    Dental pulp stem cells (DPSCs), which can differentiate into several types of cells, are subjected to mechanical stress by jaw movement and occlusal forces. In this study, we evaluated how the uniaxial mechanical stretch influences proliferation and differentiation of DPSCs. DPSCs were isolated and cultured from male Sprague-Dawley rats. Cultured DPSCs were identified by surface markers and the differentiation capabilities as adipocytes or osteoblasts. To examine the response to mechanical stress, uniaxial stretch was exposed to cultured DPSCs. We evaluated the impact of stretch on the intracellular signaling, proliferation, osteogenic differentiation, and gene expressions of DPSCs. Stretch increased the phosphorylation of Akt, ERK1/2, and p38 MAP kinase as well as the proliferation of DPSCs. The stretch-induced proliferation of DPSCs was abolished by the inhibition of the ERK pathway. On the other hand, stretch significantly decreased the osteogenic differentiation of DPSCs, but did not affect the adipogenic differentiation. We also confirmed mRNA expressions of osteocalcin and osteopontin were significantly suppressed by stretch. In conclusion, uniaxial stretch increased the proliferation of DPSCs, while suppressing osteogenic differentiation. These results suggest a crucial role of mechanical stretch in the preservation of DPSCs in dentin. Furthermore, mechanical stretch may be a useful tool for increasing the quantity of DPSCs in vitro for regenerative medicine.

    DOI: 10.1089/ten.tea.2012.0099

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  • [Musculoskeletal rehabilitation and bone. A novel approach to mechanotransduction using cell-adhesion-patterned cells]. 査読

    Katanosaka Y, Naruse K

    Clinical calcium   20 ( 4 )   514 - 519   2010年4月

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    担当区分:筆頭著者, 責任著者  

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  • A Rapid Microfluidic Switching System for Analysis at the Single Cellular Level 査読

    Akira Yamada, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse

    IEEE TRANSACTIONS ON NANOBIOSCIENCE   8 ( 4 )   306 - 311   2009年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC  

    Analysis of cellular responses to chemicals at high spatiotemporal resolution is required for precise understanding of intracellular signal transduction. Here, we demonstrated a novel method for applying different solutions to a part of or all of a cell at high spatiotemporal resolution. We fabricated a microfluidic device using polydimethylsiloxane, and the sharp interface between the two solution streams flowing in the channel was used for the application of different solutions. We constructed a computer-controlled system to control the interface movement precisely, rapidly, and reproducibly during positioning, and spatial and temporal resolutions attained were 1.6 mu m and 189 ms, respectively. We then applied the present system to the analysis of intracellular responses to chemicals. We were able to measure [Ca(2+)](i) increases within 500 ms, when one laminar stream covered a part of the cell. This method can be used as a generic platform to investigate responses against drugs at the single cell level.

    DOI: 10.1109/TNB.2009.2035253

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  • Dominant-negative inhibition of Ca2+ influx via TRPV2 ameliorates muscular dystrophy in animal models 査読

    Yuko Iwata, Yuki Katanosaka, Yuji Arai, Munekazu Shigekawa, Shigeo Wakabayashi

    HUMAN MOLECULAR GENETICS   18 ( 5 )   824 - 834   2009年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Muscular dystrophy is a severe degenerative disorder of skeletal muscle characterized by progressive muscle weakness. One subgroup of this disease is caused by a defect in the gene encoding one of the components of the dystrophin-glycoprotein complex, resulting in a significant disruption of membrane integrity and/or stability and, consequently, a sustained increase in the cytosolic Ca2+ concentration ([Ca2+](i)). In the present study, we demonstrate that muscular dystrophy is ameliorated in two animal models, dystrophin-deficient mdx mice and delta-sarcoglycan-deficient BIO14.6 hamsters by dominant-negative inhibition of the transient receptor potential cation channel, TRPV2, a principal candidate for Ca2+-entry pathways. When transgenic (Tg) mice expressing a TRPV2 mutant in muscle were crossed with mdx mice, the [Ca2+](i) increase in muscle fibers was reduced by dominant-negative inhibition of endogenous TRPV2. Furthermore, histological, biochemical and physiological indices characterizing dystrophic pathology, such as an increased number of central nuclei and fiber size variability/fibrosis/apoptosis, elevated serum creatine kinase levels, and reduced muscle performance, were all ameliorated in the mdx/Tg mice. Similar beneficial effects were also observed in the muscles of BIO14.6 hamsters infected with adenovirus carrying mutant TRPV2. We propose that TRPV2 is a principal Ca2+-entry route leading to a sustained [Ca2+](i) increase and muscle degeneration, and that it is a promising therapeutic target for the treatment of muscular dystrophy.

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  • Impairment of leukocyte deformability in patients undergoing esophagectomy 査読

    Tomohiko Suemori, Hiroshi Morimatsu, Satoshi Mizobuchi, Kiyoshi Morita, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse

    CLINICAL HEMORHEOLOGY AND MICROCIRCULATION   41 ( 2 )   127 - 136   2009年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:IOS PRESS  

    Impaired deformability might contribute to the accumulation of activated leukocytes within pulmonary microcapillaries, leading to acute lung injury. The purpose of our study was to investigate changes in leukocyte deformability during periods of inflammation after esophagectomy. The study group comprised 20 patients who underwent esophagectomy. Changes in leukocyte deformability were investigated by examining filtration through a silicon microchannel, which simulated human pulmonary microcapillaries. Changes in the neutrophil cytoskeleton were investigated by measuring neutrophil F-actin assembly. The severity of patient clinical outcome was evaluated by the lung injury score. Leukocyte filtration through the microchannel was significantly weaker in esophagectomy patients than in healthy subjects (p &lt; 0.01). After esophagectomy, filtration was further impaired compared with preoperative values (p &lt; 0.05). The neutrophil F-actin content was higher in patients than in controls (p &lt; 0.01), and increased after esophagectomy compared with preoperative values (p &lt; 0.01). We concluded that circulating leukocytes showed reduced deformability and appeared to be sequestered within microcapillaries after esophagectomy. Changes in neutrophil cytoskeleton were considered to be responsible for the reduced deformability. Leukocyte accumulation within pulmonary microcapillaries might be related to the pathogenesis of lung injury after esophagectomy.

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  • Analysis of cyclic-stretching responses using cell-adhesion-patterned cells 査読

    Yuki Katanosaka, Jin-Hua Bao, Tomoyo Komatsu, Tomohiko Suemori, Akira Yamada, Satoshi Mohri, Keiji Naruse

    JOURNAL OF BIOTECHNOLOGY   133 ( 1 )   82 - 89   2008年1月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Human vascular endothelial cells form the interface between the bloodstream and vessel walls and are continuously subjected to mechanical stimulation. When endothelial cells are stretched cyclically, along one axis, they align perpendicular to the axis of stretch. We previously reported that applying a cyclic, uni-axial strain to cells induced tyrosine phospborylation of focal adhesion kinase and stimulated mitogen-activated protein kinase. However, it is difficult to quantify and analyze the spatial distribution of tyrosine phosphorylation in these cells, as they form focal adhesions randomly. In this study, we developed a system to overcome this problem by preparing individual, uniform, patterned cells that could be stretched cyclically and uni-axially. We constructed polydimethylsiloxane stretch chambers and used microcontact printing technology to imprint a pattern of 2 mu m fibronectin dots (10 lines x 10 columns in a 38 mu m square) before seeding them with human umbilical vein endothelial cells (HUVEC). We found that most HUVEC attached to the patterned dots after 2 h and were similar in size and morphology, based on phase-contrast microscopy. In this system we were able to statistically analyze tyrosine phosphorylation and actin polymerization in these patterned cells, when subjected to a cyclic, uni-axial strain, using fluorescent microscopy. (C) 2007 Elsevier B.V. All rights reserved.

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  • Enhanced Na+/H+ exchange activity contributes to the pathogenesis of muscular dystrophy via involvement of p2 receptors 査読

    Yuko Iwata, Yuki Katanosaka, Takashi Hisamitsu, Shigeo Wakabayashi

    AMERICAN JOURNAL OF PATHOLOGY   171 ( 5 )   1576 - 1587   2007年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC INVESTIGATIVE PATHOLOGY, INC  

    A subset of muscular dystrophy is caused by genetic defects in dystrophin-associated glycoprotein complex. Using two animal models (BIO14.6 hamsters and mdx mice), we found that Na+/H+ exchanger (NHE) inhibitors prevented muscle degeneration. NHE activity was constitutively enhanced in 1310 myotubes, as evidenced by die elevated intracellular pH and enhanced Na-22(+) influx, with activation of putative upstream kinases ERK42/44. NHE inhibitor significantly reduced the increases in baseline intracellular Ca2+ as well as Na+ concentration and stretch-induced damage, suggesting that Na+ (i)-dependent Ca(2+)overload via the Na+/Ca2+ exchanger may cause muscle damage. Furthermore, ATP was found to be released continuously from BIO myotubes in a manner further stimulated by stretching and that the P2 receptor antagonists reduce the enhanced NHE activity and dystrophic muscle damage. These observations suggest that autocrine ATP release may be primarily involved in genesis of abnormal ionic homeostasis in dystrophic muscles and that Na+-dependent ion exchangers play a critical pathological role in muscular dystrophy.

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  • Heart slice NMR 査読

    Tadayuki Uetani, Daisuke Yamashita, Juichiro Shimizu, Hiromi Misawa, Yasushi Tatematsu, Yukihisa Hamaguchi, Takehiro Miyasaka, Yuki Katanosaka, Toshiaki Kato, Tatsuaki Matsubara, Koichi Furukawa, Toyoaki Murohara, Miyako Takaki, Shinsuke Nakayama

    AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY   292 ( 2 )   H1181 - H1186   2007年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    Nuclear magnetic resonance (NMR) spectroscopy of the heart is normally carried out using whole heart preparations under coronary perfusion. In such preparations, either radical changes in ionic composition of the perfusate or applications of numerous drugs would affect coronary microcirculation. This report communicates the first P-31 NMR spectroscopy study using a heart slice preparation (left ventricular slices) superfused with extracellular medium. The ratio of phosphocreatine concentration to ATP concentration was similar to 2.1. Also, intracellular pH and Mg2+ concentration ([Mg2+](i)), estimated from the chemical shifts of inorganic phosphate and ATP, were comparable with those under retrograde perfusion. [Mg2+](i) was significantly increased by the removal of extracellular Na+, supporting the essential role of Na+-coupled Mg2+ transport in Mg2+ homeostasis of the heart. Heart slice preparation could also be used to evaluate the potency of cardiac drugs, regardless of their possible effects on coronary microcirculation.

    DOI: 10.1152/ajpheart.00923.2005

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  • Regulation of the cardiac Na+/Ca2+ exchanger by calcineurin and protein kinase C 査読

    Munekazu Shigekawa, Yuki Katanosaka, Shigeo Wakabayashi

    SODIUM-CALCIUM EXCHANGE AND THE PLASMA MEMBRANE CA2+-ATPASE IN CELL FUNCTION: FIFTH INTERNATIONAL CONFERENCE   1099   53 - 63   2007年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BLACKWELL PUBLISHING  

    Na+/Ca2+ exchanger (NCX) activity is markedly inhibited in hypertrophic neonatal rat cardiomyocytes subjected to chronic phenylephrine treatment. This inhibition is reversed partially and independently by acute inhibition of calcineurin and protein kinase C (PKC) activities. Similar NCX inhibition occurs in CCL39 cells expressing cloned wildtype NCX1, when they are infected with adenoviral vectors carrying activated calcineurin A and then treated acutely with phorbol myristoyl acetate or protein phosphatase-1 inhibitors. The data obtained with these cells suggest that calcineurin activity, PKC alpha-mediated NCX1 phosphorylation, and the central loop of NCX1 (possibly its beta 1 repeat) are required for the observed NCX inhibition. We observe partial inhibition of NCX activity independent of NCX1 phosphorylation when CCL39 cells are infected with activated calcineurin A but not further treated with phorbol myristoyl acetate or phosphatase inhibitors. Calcineurin thus appears to downregulate NCX activity via two independent mechanisms, one involving NCX1 phosphorylation and the other not involving NCX1 phosphorylation. These data indicate the existence of a novel regulatory mechanism for NCX1 involving calcineurin and PKC, which may be important in cardiac pathology.

    DOI: 10.1196/annals.1387.059

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  • Phosphorylation of Na+/Ca2+ exchanger in TAB-induced cardiac hypertrophy 査読

    Yuki Katanosaka, Bongju Kim, Shigeo Wakabayashi, Satoshi Matsuoka, Munekazu Shigekawa

    SODIUM-CALCIUM EXCHANGE AND THE PLASMA MEMBRANE CA2+-ATPASE IN CELL FUNCTION: FIFTH INTERNATIONAL CONFERENCE   1099   373 - 376   2007年

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BLACKWELL PUBLISHING  

    Both protein kinase Cot-dependent Na+/Ca2+ exchanger1 (NCX1) phosphorylation and calcineurin activity are required for the depression of NCX activity observed in chronically phenylephrine (PE)treated hypertrophic neonatal rat cardiomyocytes. In this study, we explored the possibility that the same changes occur in vivo hypertrophy. In the hypertrophic hearts of thoracic aortic-banded (TAB) mice, NCX1 phosphorylation increased significantly compared with control hearts. Furthermore, the TAB-induced cardiac hypertrophy was much less prominent in transgenic mice overexpressing an NCX1 mutant having defective phosphorylation sites. These data suggest that the phosphorylation status of NCX1 may play an important role in the pathogenesis of load-induced cardiac hypertrophy.

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  • Identification and characterization of GSRP-56, a novel Golgi-localized spectrin repeat-containing protein 査読

    Yuko Kobayashi, Yuki Katanosaka, Yuko Iwata, Masayuki Matsuoka, Munekazu Shigekawa, Shigeo Wakabayashi

    EXPERIMENTAL CELL RESEARCH   312 ( 16 )   3152 - 3164   2006年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER INC  

    Spectrin repeat (SR)-containing proteins are important for regulation of integrity of biomembranes, not only the plasma membrane but also those of intracellular organelles, such as the Golgi nucleus, endo/lysosomes, and synaptic vesicles. We identified a novel SR-containing protein, named GSRP-56 (Golgi-localized SR-containing protein-56), by a yeast two-hybrid method, using a member of the transient receptor potential channel family, TRPV2, as bait. GSRP-56 is an isoform. derived from a giant SR-containing protein, Syne-1 (synaptic nuclear envelope protein-1, also referred to as Nesprin-1 or Enaptin), predicted to be produced by alternative splicing. Immunological analysis demonstrated that this isoform is a 56-kDa protein, which is localized predominantly in the Golgi apparatus in cardiomyocytes and C2C12 myoblasts/myotubes, and we found that two SR domains were required both for Golgi targeting and for interaction with TRPV2. Interestingly, overexpression of GSRP-56 resulted in a morphological change in the Golgi structure, characterized by its enlargement of cis-Golgi marker antibody-staining area, which would result partly from fragmentation of Golgi membranes. Our findings indicate that GSRP-56 is a novel, particularly small Golgi-localized member of the spectrin family, which possibly play a role in maintenance of the Golgi structure. (c) 2006 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.yexcr.2006.06.026

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  • Spatial and temporal application of microfluidics to cells 査読

    Akira Yamada, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse

    2006 IEEE INTERNATIONAL SYMPOSIUM ON MICRO-NANOMECHATRONICS AND HUMAN SCIENCE   220 - +   2006年

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    記述言語:英語   掲載種別:研究論文(国際会議プロシーディングス)   出版者・発行元:IEEE  

    The rapid solution exchange around the adhesive single cell has recently received a great deal of attention from the viewpoint cell response analyses. We recently constructed a new system, which enables the replacement of solutions rapidly and precisely, by utilizing laminar flow technology. The sharp boundary of the adjoining two liquids (no mixing) moves around the cells, and minimum increments of the boundary shift are controlled at an interval of roughly 1.6 mu m, and the time required for this movement is 20 msec. The system can be used for the analysis of intracellular Ca2+ concentrations using a fluorescent indicator, in which the cells are thus stimulated by the rapid exchange of the solution. These results suggest that the spatial and temporal control of the solution around the adhesive single cell can thus be realized.

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  • Protective effects of Ca2+ handling drugs against abnormal Ca2+ homeostasis and cell damage in myopathic skeletal muscle cells 査読

    Y Iwata, Y Katanosaka, SJ Zhu, Y Kobayashi, H Hanada, M Shigekawa, S Wakabayashi

    BIOCHEMICAL PHARMACOLOGY   70 ( 5 )   740 - 751   2005年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Deficiency of delta-sarcoglycan (delta-SG), a component of the dystrophin-glycoprotein complex (DGC), causes skeletal muscular dystrophy and cardiomyopathy in BIO14.6 hamsters. Here, we studied the involvement of abnormal Ca2+ homeostasis in muscle degeneration and the protective effect of drugs against Ca2+ handling proteins in vivo as well as in vitro. First, we characterized the properties of cultured myotubes from muscles of normal and BIO14.6 hamsters (30-60 days old). While there were no apparent differences in the levels of expression of various Ca2+ handling proteins (L-type Ca2+ channel, ryanodine receptor, SR-Ca2+ ATPase, and Na+/Ca2+ exchanger), muscle-specific proteins (contractile actin and acetylcholine receptor), or DGC member proteins except SGs, BIO14.6 myotubes showed a high degree of susceptibility to mechanical stressors, such as cyclic stretching and hypo-osmotic stress as compared to normal myotubes, as evidenced by marked increases in creatine phosphokinase (CK) release and bleb formation. BIO14.6 myotubes showed abnormal Ca2+ homeostasis characterized by elevated cytosolic Ca2+ concentration, frequent Ca2+ oscillation, and increased 45 Ca2+ uptake. These abnormal Ca2+ events and CK release were significantly prevented by Ca2+ handling drugs, tranilast, diltiazem, and FK506. The calpain inhibitor E64 prevented CK release, but not Ca-45(2+) uptake. Some of these drugs (tranilast, diltiazem, and FK506) also exerted a significant protective effect for muscle degeneration in BIO14.6 hamsters and mdx mice in vivo. These observations suggest that elevated Ca2+ entry through sarcolemmal Ca2+ channels predominantly contributes to muscle degeneration and that the drugs tested here may have novel therapeutic potential against muscular dystrophy. (c) 2005 Elsevier Inc. All rights reserved.

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  • Mitochondrial dysfunction is related to necrosis-like programmed cell death induced by A23187 in CEM cells 査読

    K Hamahata, S Adachi, H Matsubara, M Okada, T Imai, K Watanabe, S Toyokuni, M Ueno, S Wakabayashi, Y Katanosaka, S Akiba, M Kubota, T Nakahata

    EUROPEAN JOURNAL OF PHARMACOLOGY   516 ( 3 )   187 - 196   2005年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    We have previously reported that calcium ionophore A23187 differentially induces necrosis in CEM cells, a T-lymphoblastic leukemia cell line, and apoptosis in HL60 cells, a promyclocytic leukemia cell line. Stimulation with VP16, however, induces typical apoptosis in both cell lilies. Necrosis in CEM cells, characterizedby cell shrinkage and clustering, began within 5 min of treatment. Swelling of the mitochondria, lumpy chromatin condensation and intact plasma membranes were evident by electron microscopy. These A23187-illediated changes in CEM cells were suppressed by clonazepam or CGP37157, inhibitors of the mitochondrial Na+/Ca2+ exchanger. The changes, however, were not affected by cyclosporin A, an inhibitor of the mitochondrial permeability transition pore. In both CEM and HL60 cells, intra-cellular calcium increased with similar amplitude within 1 min of treatment with 2 mu M A23187. Intra-mitochondrial calcium increased with clonazepam pre-treatment alone in both CEM and HL60 cells. However, intra-mitochondrial calcium did not change drastically in response to A23187 in CEM or HL60 cells, either untreated or pre-treated with clonazepam. A23187 induces necrosis in CEM cells concurrent with mitochondrial dysfunction, which is independent of the mitochondrial permeability transition, but affected by intra-mitochondrial calcium, while HL60 cells lack these early changes. Differences in the responses to A23187 between these two cell lilies might derive from differences in the susceptibility of the mitochondrial membrane to rapid increases in intra-cellular calcium. (c) 2005 Elsevier B.V All rights reserved.

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  • Calcineurin inhibits Na+/Ca2+ exchange in phenylephrine-treated hypertrophic cardiomyocytes 査読

    Y Katanosaka, Y Iwata, Y Kobayashi, F Shibasaki, S Wakabayashi, M Shigekawa

    JOURNAL OF BIOLOGICAL CHEMISTRY   280 ( 7 )   5764 - 5772   2005年2月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    The cardiac Na+/Ca2+ exchanger (NCX1) is the predominant mechanism for the extrusion of Ca2+ from beating cardiomyocytes. The role of protein phosphorylation in the regulation of NCX1 function in normal and diseased hearts remains unclear. In our search for proteins that interact with NCX1 using a yeast two-hybrid screen, we found that the C terminus of calcineurin Abeta, containing the autoinhibitory domain, binds to the beta1 repeat of the central cytoplasmic loop of NCX1 that presumably constitutes part of the allosterie Ca2+ regulatory site. The association of NCX1 with calcineurin was significantly increased in the BI014.6 cardiomyopathic hamster heart compared with that in the normal control. In hypertrophic neonatal rat cardiomyocytes subjected to chronic phenylephrine treatment, we observed a marked depression of NCX activity measured as the rate of Na+ i-dependent Ca-45(2+) uptake or the rate of Na+ o-dependent Ca-45(2+) efflux. Depressed NCX activity was partially and independently reversed by the acute inhibition of calcineurin and protein kinase C activities with little effect on myocyte hypertrophic phenotypes. Studies of NCX1 deletion mutants expressed in CCL39 cells were consistent with the view that the beta1. repeat is required for the action of endogenous calcineurin and that the large cytoplasmic loop may be required to maintain the interaction of the enzyme with its substrate. Our data suggest that NCX1 is a novel regulatory target for calcineurin and that depressed NCX activity might contribute to the etiology of in vivo cardiac hypertrophy and dysfunction occurring under conditions in which both calcineurin and protein kinase C are chronically activated.

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  • Association of genetic polymorphisms of sodium-calcium exchanger 1 gene, NCX1, with hypertension in a Japanese general population 査読

    Y Kokubo, N Inamoto, H Tomoike, K Kamide, S Takiuchi, Y Kawano, C Tanaka, Y Katanosaka, S Wakabayashi, M Shigekawa, O Hishikawa, T Miyata

    HYPERTENSION RESEARCH   27 ( 10 )   697 - 702   2004年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPANESE SOC HYPERTENSION CENT ACADEMIC SOC, PUBL OFFICE  

    The Na+/Ca2+ exchanger (NCX) is a membrane protein involved in calcium homeostasis, catalyzing the exchange of one Ca2+ ion for three Na+ ions across the cell membrane. The Na+/Ca2+ exchange has been suggested to play a role in the pathogenesis of hypertension. Therefore, we examined whether genetic variations in NCX1 were associated with hypertension. Among 15 polymorphisms identified in 96 hypertensive subjects by sequencing the entire exon and promoter regions of NCX1, 7 representative polymorphisms with a minor allele frequency of greater than 4% were genotyped in 1,865 individuals, of whom 787 were hypertensive and 1,072 were normotensive. These subjects were residents of Suita City and were randomly selected as a population for the Suita cohort study. Multivariate logistic regression analysis performed after adjusting for age, body mass index, hyperlipidemia, diabetes mellitus, smoking, and drinking revealed that the -23200T &gt; C and -23181T &gt; C polymorphisms in the 5'upstream region of exon 1c were significantly associated with hypertension in men (-23200T &gt; C: CC vs. TC+TT: odds ratio = 0.61; 95% confidence intervals: 0.39 to 0.97; p = 0.04) and in women (-23181T &gt; C: CC vs. TC+TT: odds ratio = 1.45; 95% confidence intervals: 1.04 to 2.02; p = 0.03), respectively. Thus, our study suggests that NCX1 is one of the genes related to susceptibility to essential hypertension in the Japanese general population.

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  • TRPV2 is a component of osmotically sensitive cation channels in murine aortic myocytes 査読

    K Muraki, Y Iwata, Y Katanosaka, T Ito, S Ohya, M Shigekawa, Y Imaizumi

    CIRCULATION RESEARCH   93 ( 9 )   829 - 838   2003年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Changes in membrane tension resulting from membrane stretch represent one of the key elements in blood flow regulation in vascular smooth muscle. However, the molecular mechanisms involved in the regulation of membrane stretch remain unclear. In this study, we provide evidence that a vanilloid receptor (TRPV) homologue, TRPV2 is expressed in vascular smooth muscle cells, and demonstrate that it can be activated by membrane stretch. Cell swelling caused by hypotonic solutions activated a nonselective cation channel current (NSCC) and elevated intracellular Ca2+ ([Ca2+](i)) in freshly isolated cells from mouse aorta. Both of these signals were blocked by ruthenium red, an effective blocker of TRPVs. The absence of external Ca2+ abolished this increase in [Ca2+](i) caused by the hypotonic stimulation and reduced the activation of NSCC. Significant immunoreactivity to mouse TRPV2 protein was detected in single mouse aortic myocytes. Moreover, the expression of TRPV2 was found in mesenteric and basilar arterial myocytes. Treatment of mouse aorta with TRPV2 antisense oligonucleotides resulted in suppression of hypotonic stimulation-induced activation of NSCC and elevation of [Ca2+](i) as well as marked inhibition of TRPV2 protein expression. In Chinese hamster ovary K1 (CHO) cells transfected with TRPV2 cDNA (TRPV2-CHO), application of membrane stretch through the recording pipette and hypotonic stimulation consistently activated single NSCC. Moreover, stretch of TRPV2-CHO cells cultured on an elastic silicon membrane significantly elevated [Ca2+](i). These results provide a strong basis for our purpose that endogenous TRPV2 in mouse vascular myocytes functions as a novel and important stretch sensor in vascular smooth muscles.

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  • A novel mechanism of myocyte degeneration involving the Ca2+-permeable growth factor-regulated channel 査読

    Y Iwata, Y Katanosaka, Y Arai, K Komamura, K Miyatake, M Shigekawa

    JOURNAL OF CELL BIOLOGY   161 ( 5 )   957 - 967   2003年6月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ROCKEFELLER UNIV PRESS  

    Disruption of the dystrophin-glycoprotein complex caused by genetic defects of dystrophin or sarcoglycans results in muscular dystrophy and/or cardiomyopathy in humans and animal models. However, the key early molecular events leading to myocyte degeneration remain elusive. Here, we observed that the growth factor-regulated channel (GRC), which belongs to the transient receptor potential channel family, is elevated in the sarcolemma of skeletal and/or cardiac muscle in dystrophic human patients and animal models deficient in dystrophin or delta-sarcoglycan. However, total cell GRC does not differ markedly between normal and dystrophic muscles. Analysis of the properties of myotubes prepared from delta-sarcoglycan-deficient BIO14.6 hamsters revealed that GRC is activated in response to myocyte stretch and is responsible for enhanced Ca2+ influx and resultant cell damage as measured by creatine phosphokinase efflux. We found that cell stretch increases GRC translocation to the sarcolemma, which requires entry of external Ca2+. Consistent with these findings, cardiac-specific expression of GRC in a transgenic mouse model produced cardiomyopathy due to Ca2+ overloading, with disease expression roughly parallel to sarcolemmal GRC levels. The results suggest that GRC is a key player in the pathogenesis of myocyte degeneration caused by dystrophin-glycoprotein complex disruption.

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  • Pinopsin expressed in the retinal photoreceptors of a diurnal gecko 査読

    Y Taniguchi, O Hisatomi, M Yoshida, F Tokunaga

    FEBS LETTERS   496 ( 2-3 )   69 - 74   2001年5月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Retinal cDNAs encoding the putative opsins, dg3 and dg4, were isolated from a diurnal gecko, Phelsuma madagascariensis longinsulae, dg3 mRNA is localized in about 20% of the Chin members of type C double cones, and likely encodes an opsin of the ultraviolet-sensitive pigment. Surprisingly, dg4 is very similar to chicken pinopsin, a pineal-specific photoreceptive molecule, An anti-dg4 antiserum recognized a small population of photoreceptor outer segments in the retina and a large number of pinealocytes. Our results suggest that P. m. longinsulae expresses pinopsin in its retina, which usually plays a role as a photoreceptive molecule in the pineal organ, (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

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  • Primary structure of a visual pigment in bullfrog green rods 査読

    O Hisatomi, Y Takahashi, Y Taniguchi, Y Tsukahara, F Tokunaga

    FEBS LETTERS   447 ( 1 )   44 - 48   1999年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    In frog retina there are special rod photoreceptor cells ('green rods') with physiological properties similar to those of typical vertebrate rods ('red rods'). A cDNA fragment encoding the putative green rod visual pigment,vas isolated from a retinal cDNA. library of the bullfrog, Rana catesbeiana. Its deduced amino acid sequence has more than 65% identity with those of blue-sensitive cone pigments such as chicken blue and goldfish blue, Antisera raised against its C-terminal amino acid sequence recognized green rods. It is concluded that bullfrog green rods contain a visual pigment which is closely related to the blue-sensitive cone pigments of other non-mammalian vertebrates. (C) 1999 Federation of European Biochemical Societies.

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  • Evolution of visual pigments in geckos 査読

    Y Taniguchi, O Hisatomi, M Yoshida, F Tokunaga

    FEBS LETTERS   445 ( 1 )   36 - 40   1999年2月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Most geckos are nocturnal forms and possess rod retinas, but some diurnal genera have pure-cane retinas, We isolated cDNAs encoding the diurnal gecko opsins, dg1 and dg2, similar to nocturnal gecko P521 and P467, respectively, Despite the large morphological differences between the diurnal and nocturnal gecko photoreceptor types, they express phylogenetically closely related opsins. These results provide molecular evidence for the reverse transmutation, that is, rods of an ancestral nocturnal gecko have backed into cones of diurnal geckos, The amino acid substitution rates of dg1 and dg2 are higher than those of P521 and P467, respectively, Changes of behavior regarding photic environment may have contributed to acceleration of amino acid substitutions in the diurnal gecko opsins (C) 1999 Federation of European Biochemical Societies.

    DOI: 10.1016/S0014-5793(99)00089-7

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  • Evolution of visual pigments and related molecules 査読

    Fumio Tokunaga, Osamu Hisatomi, Takunori Satoh, Yuki Taniguchi, Shinji Matsuda, Yoshikazu Imanishi, Hanayo Honkawa, Yusuke Takahashi, Yuko Kobayashi, Masao Yoshida, Yasuo Tsukahara

    Novartis Foundation Symposium   224   44 - 53   1999年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The molecular phylogenetic tree of vertebrate visual pigments, constructed on the basis of amino acid sequence identity, suggests that the visual pigments can be classified into five groups (L, ML, MS, S and Rh) and that their genes have evolved along these five gene lines. Goldfish has a UV-sensitive visual pigment (S group) localized in miniature single cone cells. Medaka has one type of rod cell containing rhodopsin (Rh group) and four types of cone cells, each of which contains a specific visual pigment with an absorption maximum that differs from those of the others. Frogs have a violet-sensitive visual pigment (S group) in small single cone cells and a blue-sensitive visual pigment (MS group) in green rod cells. Although nocturnal and diurnal geckos have rod- and cone-based retinas, respectively, they have phylogenetically closely related visual pigments. The pigments in each line may have restricted absorption maxima. We have cloned cDNAs encoding molecules involved in the phototransduction system of visual cells, such as phosphodiesterase, opsin kinase and arrestin. We then constructed phylogenetic trees of these molecules with the deduced amino acid sequences. The resulting phylogenetic trees show that these molecules are classified into two groups
    one is expressed in cones and another in rods, suggesting that rods and cones contain homologous molecules with different amino acid sequences. These differences may result in the different light responses of rods and cones.

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  • Primary structure and characterization of a bullfrog visual pigment contained in small single cones. 査読 国際誌

    Hisatomi O, Kayada S, Taniguchi Y, Kobayashi Y, Satoh T, Tokunaga F

    Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology   119 ( 3 )   585 - 591   1998年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/S0305-0491(98)00032-7

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MISC

  • 筋ジストロフィー関連心筋症でみられるゴルジ異常と微小管過重合 招待

    片野坂友紀

    医学のあゆみ   278 ( 3 )   231 - 232   2021年

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    担当区分:筆頭著者, 責任著者  

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  • TRPV2を核とした心臓のメカノバイオロジー研究

    片野坂 友紀

    医学のあゆみ   270 ( 10 )   904 - 909   2019年9月

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  • TRPシグナルを利用した機械受容~心臓の可塑性や生理機能を支えるTRPチャネルを中心に~ 招待

    片野坂 友紀

    医学のあゆみ   257   1015 - 1022   2016年

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    記述言語:日本語  

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  • The Generation of a Novel Animal Model of Inducible Hypertrophy: Overexpression of NCX1 in the Murine Heart Using the Doxycycline-Dependent Promoter

    Yuki Katanosaka, Keiichiro Iwasaki, Satoshi Mohri, Keiji Naruse

    BIOPHYSICAL JOURNAL   98 ( 3 )   551A - 551A   2010年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:CELL PRESS  

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  • 新しい伸展刺激負荷方法を用いたメカノトランスダクション研究 招待

    片野坂 友紀, 成瀬恵治

    血管医学   11   41 - 46   2010年

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    記述言語:日本語  

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  • STRETCH-INDUCED UP-REGULATION OF SOC ACTIVITIES IN HUVEC

    Yuki Katanosaka, Keiji Naruse

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   500 - 500   2009年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER TOKYO  

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  • メカニカルストレスに対する細胞応答の解析技術 招待

    片野坂 友紀, 竹内崇, 成瀬恵治

    次世代医療のための高分子材料工学   158 - 167   2008年

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    記述言語:日本語  

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  • The role of TRP channels in mechanotransduction of HUVEC

    Yuki Katanosaka, Tomohiko Suemori, Keiji Naruse

    BIOPHYSICAL JOURNAL   291A - 291A   2007年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:BIOPHYSICAL SOCIETY  

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  • ヒト臍帯血血管内皮細胞(HUVEC)のストレッチ刺激に対する細胞応答

    片野坂友紀, 成瀬恵治

    医学のあゆみ   223 ( 6 )   469 - 473   2007年

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  • Na+/H+ exchange inhibitors protect against muscle degeneration in cardiomyopathic hamsters

    Yuko Iwata, Yuki Katanosaka, Shigeo Wakabayashi

    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY   40 ( 6 )   952 - 952   2006年6月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    DOI: 10.1016/j.yjmcc.2006.03.103

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  • The phosphorylation and inhibition of Na+/Ca2+ exchanger in phenylephrin-treated hypertrophic cardiomyocytes

    Yuki Katanosaka, Yuko Iwata, Shigeo Wakabayashi, Munekazu Shigekawa

    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY   40 ( 6 )   951 - 951   2006年6月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    DOI: 10.1016/j.yjmcc.2006.03.100

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  • Cardiac Na+/Ca2+ exchanger is highly phosphorylated and inhibited by PKC alpha in phenylephrin-treated hypertrophic cardiomyocytes

    Y Katanosaka, Y Iwata, M Shigekawa, S Wakabayashi

    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY   39 ( 6 )   1023 - 1024   2005年12月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

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  • Mechanism of myocyte degeneration II: transgenic cardiac expression of stretch-activated non-selective cation chanel grc leads to myocardial hypertrophy and failure

    Y Katanosaka, Y Iwata, K Komamura, S Wakabayashi, M Shigekawa

    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY   38 ( 6 )   1033 - 1033   2005年6月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

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  • Mechanism of myocyte degeneration II: Transgenic cardiac expression of stretch-activated nonselective cation channel GRC leads to myocardial hypertrophy and failure.

    Y Katanosaka, Y Iwata, K Komamura, S Wakabayashi, M Shigekawa

    BIOPHYSICAL JOURNAL   88 ( 1 )   495A - 495A   2005年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:BIOPHYSICAL SOCIETY  

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  • Mechanism of myocyte degeneration I: A novel target for muscle dystrophy and cardiomyopathy

    Y Iwata, Y Katanosaka, S Wakabayashi, M Shigekawa

    BIOPHYSICAL JOURNAL   88 ( 1 )   495A - 495A   2005年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:BIOPHYSICAL SOCIETY  

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講演・口頭発表等

  • 細径線維受容器終末のTRPV2チャネルを介した機械痛覚の末梢神経機構

    田口徹, 片野坂友紀, 太田大樹, 片野坂公明

    日本基礎理学療法学会  2021年10月23日 

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  • Analysis of Molecular Mechanisms Involved in Mechanical Adaptation: In the Case of Repeated Bout Effect on the Exercise-induced Muscle Pain.

    Yuhei Hibino, Yuki Katanosaka, Kimiaki Katanosaka

    The 3rd International Yangtze River Delta Symposium on Mechanobiology & the 9th Chinese National Symposium of Medical Biophysics  2021年10月16日 

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  • TRPV2 is Involved in the Hypertrophic Response of Skeletal Muscle Induced by Mechanical Overload

    Yuki Katanosaka, Chen Yanzhu, Dong Yubing, Makoto Shibuya, Keiji Narus

    The 3rd International Yangtze River Delta Symposium on Mechanobiology & the 9th Chinese National Symposium of Medical Biophysics  2021年10月16日 

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  • The Role of TRPV2 in cardiovascular systems

    Yuki Katanosaka

    The 4th international TRP meeting (inveited)  2021年9月16日 

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  • TRPA1 contributes to lengthening contraction-induced muscular mechanical hyperalgesia

    Hiroaki Ota, Washizawa Leo, Hayashi Koei, Yuki Katanosaka, Kimiaki Katanosaka, Makoto Tominaga, Toru Taguchi, Kazue Mizumura

    The 4th international TRP meeting  2021年9月15日 

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  • ダイナミン1は微小管の配向を調節しTRPV2の細胞膜移行を制御する

    籔彩夏, 安岡宏樹, 片野坂友紀, 阿部匡史, 竹田哲也, 竹居孝二, 山田浩司

    生化学会中四国支部会  2021年9月10日 

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  • Involvement of TRPA1 but not TRPV2 in rodent models of lengthening contraction-induced muscular mechanical hyperalgesia

    Hiroki Ota, Leo Washizawa, Kohei Hayashi, Yuki Katanosaka, Kimiaki Kaanosaka, Makoto Tominaga, Toru Taguchi, Kazue Mizumura

    日本神経科学会大会  2021年7月28日 

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  • The role of TRPV2 in cardiac physiology and cardiovascular disease

    Yuki Katanosaka

    日本生体医工学会 シンポジウム  2021年6月16日 

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  • 生理的・病的リモデリングにおけるメカノセンサーTRPV2の役割

    片野坂友紀

    日本薬理学会 企画シンポジウム  2021年3月 

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  • TRPV2 Promotes Hypoxia-induced Pulmonary Hypertension

    Kazufumi Nakamura, Yuki Katanosaka, Satoshi Akagi, Yukihiro Saito, Kentaro Ejiri, Toru Miyoshi, Masashi Yoshida, Satoshi Hirohata, Hiroshi Ito

    日本循環器学会  2021年 

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  • マウス遅発性筋痛モデルにおけるTRPチャネルの関与

    太田大樹, 片野坂公明, 村瀬詩織, 加塩麻紀子, 富永真琴, 片野坂友紀, 田口徹, 水村和枝

    第25回日本基礎理学療法学術大会  2020年12月12日 

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  • 皮膚の機械痛覚におけるTRPV2の関与:単一神経記録法による電気生理学的解析

    田口徹, 片野坂友紀, 片野坂公明

    第42回日本疼痛学会  2020年12月4日 

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  • 遅発性筋痛の分子機構: TRPA1およびTRPV2ノックアウトマウスを用いた解析

    太田大樹, 片野坂公明, 村瀬詩織, 加塩麻紀子, 富永真琴, 片野坂友紀, 田口徹, 水村和枝

    第42回日本疼痛学会  2020年12月4日 

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  • 筋機能維持におけるTRPV2の役割

    片野坂友紀

    日本分子生物学会 シンポジウム  2020年12月 

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  • マウス遅発性筋痛モデルにおける機械感受性TRPチャネルの関与

    太田大樹, 片野坂公明, 村瀬詩織, 加塩麻紀子, 富永真琴, 片野坂友紀, 田口徹, 水村和枝

    第13回日本運動器疼痛学会  2020年11月28日 

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  • 圧負荷によって引き起こされる心不全における心血管TRPV2の役割

    片野坂友紀

    日本脈管学会総会 シンポジウム  2020年11月 

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  • Decreased mechanical response of cutaneous nociceptors in TRPV2-deficient mice

    Toru Taguchi, Yuki Katanosaka, Kimiaki Katanosaka

    43rd Annual Meeting of the Japan Neuroscience Society  2020年7月29日 

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  • The molecular mechanism of cardiac mechanical response in physiology and pathophysiology

    片野坂友紀

    日本生体医工学会 シンポジウム  2020年6月 

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  • 心臓のメカノバイオロジー ~心筋細胞のTRPV2の役割を中心に~ 招待

    片野坂 友紀

    日本高血圧学会 シンポジウム  2019年11月 

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    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • 骨格筋特異的TRPV2ノックアウトマウスを用いたメカニカルストレス応答の解析

    第7回若手による骨格筋細胞研究会  2019年10月 

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  • 骨格筋特異的TRPV2ノックアウトマウスを用いたメカニカルストレス応答の解析

    片野坂友紀

    日本メカノバイオロジー研究会  2019年9月 

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  • 興奮収縮連関獲得におけるTRPV2の役割

    Yuki Katanosaka

    Gordon conference (Italy)  2019年6月 

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  • 心臓の可塑性や生理機能を支える膜輸送体:メカノセンサーTRPV2 招待

    片野坂 友紀

    日本生理学会 シンポジウム  2018年9月 

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    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

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  • Fukutin-KO心筋細胞から探る筋ジストロフィー関連心筋症の病態発症メカニズム 招待

    片野坂 友紀

    日本筋学会  2018年8月 

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    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • 心臓の分化・成熟およびストレス応答におけるメカノセンサーTRPV2の役割 招待

    片野坂 友紀

    日本生体医工学会  2018年6月 

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    記述言語:日本語  

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  • Critical roles for TRPV2 in the formation and maintenance of intercalated discs in cardiomyocytes 招待

    片野坂 友紀

    日本生理学会  2018年3月 

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    記述言語:英語  

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  • TRPV2は、新生児心筋細胞の興奮収縮連関獲得に必要である

    Biophysics (USA)  2018年2月 

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  • Fukutin KO心筋細胞から探る筋ジストロフィー関連症の病態発症メカニズム

    片野坂 友紀

    若手による若手による骨格筋細胞研究会  2017年10月 

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    記述言語:日本語  

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  • TRPV2 is required for the normal cardiac plasticity 招待

    片野坂 友紀

    日本生理学会  2017年3月 

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    記述言語:英語  

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  • The role of TRPV2 in the heart 招待

    片野坂 友紀

    2017年3月 

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    記述言語:日本語  

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  • The critical role of TRPV2 within the working heart 招待

    片野坂 友紀

    日本生体医工学会大会  2016年5月 

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    記述言語:日本語  

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  • TRPV2 is crucial for cardiac structure and function. 招待

    片野坂 友紀

    日本薬理学会  2015年3月 

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    記述言語:英語  

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  • メカニカルストレスを利用した筋細胞の機能維持 招待

    片野坂 友紀

    日本生化学会  2014年10月 

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    記述言語:日本語  

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産業財産権

  • 筋ジストロフィー関連心筋症の治療又は予防剤

    片野坂友紀

     詳細を見る

    出願人:国立大学法人 岡山大学

    出願番号:PCT/JP2019/9742  出願日:2019年3月11日

  • 骨格筋特異的TRPV2ノックアウトマウス非ヒト動物

    片野坂友紀

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    出願人:国立大学法人 岡山大学

    出願番号:特願2017-165196  出願日:2017年8月30日

  • 特許第6923186号(平滑筋特異的TRPV2ノックアウトマウス非ヒト動物)

    片野坂友紀

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    出願人:国立大学法人 岡山大学

    出願番号:特願2017-073994  出願日:2017年4月3日

共同研究・競争的資金等の研究

  • 筋細胞の恒常性維持におけるメカノセンサーの役割

    2021年11月 - 現在

    三菱財団自然科学研究 研究助成 

  • 心筋細胞のメカノトランスダクションに基づく心不全新規治療ターゲットの確立 :内因性ペプチド・Apelinを用いた医療技術の開発

    2021年11月 - 現在

    鈴木謙三記念医科学応用研究財団 助成金 

  • 心血管メカノセンサーTRPV2の低酸素誘発性肺高血圧症への関与解明と治療法開発

    2021年04月 - 現在

    文科省科研費・基盤C 

  • 大動脈解離におけるメカノバイオロジー機構の解明

    2021年04月 - 現在

    文科省科研費・基盤C 

  • 福山型筋ジストロフィーおよび類縁の糖鎖異常型筋ジストロフィーに対する糖鎖補充療法の開発 

    2020年10月 - 現在

    難治性疾患実用化研究事業 

  • 遅発性筋痛における機械感受性イオンチャネルの役割の解明

    2020年04月 - 現在

    文科省科研費・基盤C  基盤C

  • 心不全発症におけるメカノセンサー分子の役割

    2019年10月 - 2021年10月

    アステラス病態代謝研究会 研究助成 

  • 筋ジストロフィー関連心筋症における微小管過重合の改善による 新規治療法の開発

    2019年10月 - 2020年10月

    加藤記念年病研究助成基金研究 

  • 機械受容応答を支える膜・糖鎖環境の解明と筋疾患治療への展開  

    2019年04月 - 現在

    革新的先端研究開発支援事業  

  • 心筋細胞の介在板から入力するメカニカルシグナルの可視化

    2018年04月 - 2020年03月

    JSPS  文科省科研費・挑戦的萌芽 

    片野坂 友紀

      詳細を見る

    担当区分:研究代表者  資金種別:競争的資金

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  • 多階層医工学的解析に基づくメカニカルストレスを利用した心機能維持の分子基盤の解明

    2017年04月 - 2020年03月

    JSPS  文科省科学研究費・基盤B 

    片野坂 友紀

      詳細を見る

    担当区分:研究代表者  資金種別:競争的資金

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  • 生体の機械受容機構の分子基盤と生理的意義の解明による革新的医療ターゲットの確立

    2015年12月 - 2019年03月

    AMED  革新的先端研究開発支援事業 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 多階層医工学的解析に基づく心臓の機械受容システムの分子基盤と生理学的意義の解明

    2014年04月 - 2017年03月

    JSPS  文科省科学研究費・基盤B 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 心機能を支える臓器間連関の解明による新しい心不全治療の開発

    2013年04月 - 2015年03月

    JSPS  文科省科学研究費・挑戦的萌芽 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • メカニカルストレスを利用した生体の巧みな適応機構と破綻システムの解明

    2011年01月 - 2014年03月

    内閣府  最先端・次世代研究開発プロジェクト 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • マルチレベル医工学評価法に基づく心筋メカノセンサーの作動機序と病態生理的役割

    2009年04月 - 2012年03月

    JSPS  文科省科学研究費・基盤B 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 医工学的解析に基づく肺ストレッチセンサーを介した肺癌発症機構の解明

    2009年04月 - 2011年03月

    JSPS  文科省科学研究費・挑戦的萌芽 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 生体メカノセンサーの制御操作による新規心不全治療の開発

    2008年04月 - 2010年03月

    JSPS  文部省科学研究費特定研究 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 心不全におけるCa2+ハンドリング機構解明と是正治療の開発

    2007年04月 - 2010年03月

    JSPS  文科省科学研究費・若手B 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 心不全発症におけるNa+/Ca2+交換体の役割

    2006年03月

    JSPS  日本学術振興会特別研究員SPD 研究奨励金 

    片野坂 友紀

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    担当区分:研究代表者  資金種別:競争的資金

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  • 拍動する心臓におけるメカノセンサーの活性化をモニターする挑戦的研究

    挑戦的研究(開拓)

    片野坂友紀

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▼全件表示

その他研究活動

  • TRPV2ノックアウトマウスを用いた発生研究

    2019年04月
    -
    現在

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    TRPV2ノックアウトマウスを用いたベルギーTRP研究所との共同研究

 

担当授業科目

  • システム生理学I(演習・実習) (2021年度) 特別  - その他

  • システム生理学I(講義・演習) (2021年度) 特別  - その他

  • システム生理学II(演習・実習) (2021年度) 特別  - その他

  • システム生理学II(講義・演習) (2021年度) 特別  - その他

  • 人体生理学 (2021年度) 集中  - その他

  • 医学セミナー (2021年度) 第1学期

  • 医学研究インターンシップ (2021年度) 特別

  • 基礎病態演習 (2021年度) 特別

  • 生理学Ⅱ (2021年度) 特別  - その他

  • 生理学Ⅱ実習 (2021年度) 特別  - その他

  • システム生理学I(演習・実習) (2020年度) 特別  - その他

  • システム生理学I(講義・演習) (2020年度) 特別  - その他

  • システム生理学II(演習・実習) (2020年度) 特別  - その他

  • システム生理学II(講義・演習) (2020年度) 特別  - その他

  • 人体生理学 (2020年度) 集中  - その他

  • 生理学Ⅱ (2020年度) 特別  - その他

  • 生理学Ⅱ実習 (2020年度) 特別  - その他

▼全件表示

 

メディア報道

  • NHK-BS ヒューマニエンス 心臓 「“心臓” 心が宿る もう一人の私」

    NHKーBS  2021年1月14日

  • NHK おはよう日本 (筋ジストロフィー症発症のしくみ)

    NHK  2020年

  • 心臓の構造や機能を維持する仕組みを解明 新聞・雑誌

    山陽新聞・日本経済新聞  2014年

学術貢献活動

  • 生体医工学会 シンポジウム

    役割:パネル司会・セッションチェア等

    2020年6月

  • 文科省科研費審査員

    役割:審査・評価

    2019年 - 現在

     詳細を見る

    種別:審査・学術的助言 

  • 日本生理学会 入澤彩記念女性生理学者奨励賞審査委員

    役割:審査・評価

    2019年

  • NISTEP専門調査員

    役割:学術調査立案・実施

    2018年4月1日 - 2020年3月31日

  • 論文査読

    役割:査読

    2007年4月16日 - 現在