Fluorescence Analysis of the Mitochondrial Effect of a Plasmalemmal Na⁺/Ca²⁺ Exchanger Inhibitor, SEA0400, in Permeabilized H9c2 Cardiomyocytes

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  • Namekata Iyuki
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Hamaguchi Shogo
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Iida-Tanaka Naoko
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University Department of Food Science, Otsuma Women’s University
  • Kusakabe Taichi
    Department of Organic Chemistry, Faculty of Pharmaceutical Sciences, Toho University
  • Kato Keisuke
    Department of Organic Chemistry, Faculty of Pharmaceutical Sciences, Toho University
  • Kawanishi Toru
    National Institute of Health Sciences
  • Tanaka Hikaru
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University

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タイトル別名
  • Fluorescence Analysis of the Mitochondrial Effect of a Plasmalemmal Na<sup>+</sup>/Ca<sup>2+</sup> Exchanger Inhibitor, SEA0400, in Permeabilized H9c2 Cardiomyocytes

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<p>We investigated the effect on mitochondrial Ca2+ of SEA0400, an inhibitor of the Na+/Ca2+ exchanger (NCX) which reduces mitochondrial Ca2+ overload during myocardial ischemia, in digitonin-permeabilized H9c2 cells expressing the mitochondrial-targeted Ca2+ indicator, yellow cameleon 3.1. The elevation of mitochondrial Ca2+ concentration caused by an increase in extramitochondrial Ca2+ concentration was inhibited by carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) or ruthenium red, but enhanced by CGP-37157, a mitochondrial NCX inhibitor. SEA0400 had no effect on mitochondrial Ca2+ under normal and ischemic conditions. Thus, the mitochondria-protective effects of SEA0400 could be explained by inhibition of plasmalemmal NCX but not mitochondrial NCX.</p>

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