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Myocardial preservation specific for cardiomyocytes

Research Project

Project/Area Number 16591420
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Thoracic surgery
Research InstitutionKansai Medical University

Principal Investigator

OTANI Hajime  Kansai Medical University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (60168979)

Co-Investigator(Kenkyū-buntansha) SUMIDA Tomohiko  Kansai Medical University, Faculty of Medicine, 医学部, 助手 (00319625)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
KeywordsDystrophin / Heart / Ischemia / Reperfusion / Ischemic preconditioning / Mitochondria
Research Abstract

Objective : Dystrophin is a membrane protein that protects the sarcolemma from oncosis induced by physical stress. Because ischemic preconditioning (IPC) protects mitochondria and prevents oncosis during reperfusion, we hypothesized that dystrophin is a target of IPC distal to mitochondrial protection. Methods and Results : The isolated rat hearts were subjected to 30 minutes ischemia followed by reperfusion. IPC was introduced by 3 cycles of 5 minutes ischemia and 5 minutes reperfusion. The loss of sarcolemmal dystrophin and myocardial ATP during ischemia was similar in the control and the IPC heart. Similar loss of sarcolemmal dystrophin and myocardial ATP was observed when the heart was treated with 2,4-dinitrophenol (DNP), an uncoupler of mitochondrial respiration, or oligomycin, an inhibitor of mitochondrial F_1F_0-ATPase. However, the IPC heart increased sarcolemmal dystrophin during reperfusion associated with an increase in tetramethylrhodamine ethylester (TMRE) uptake, an indicator of mitochondrial membrane potential (Δψm), and myocardial ATP and inhibition of myocyte oncosis. The increase in relocalization of sarcolemmal dystrophin and myocardial ATP mediated by IPC was inhibited by treatment with DNP or oligomycin during reperfusion. Moreover, the ischemic IPC heart mitochondria increased relocalization of dystrophin from the insoluble to the soluble fractions associated with increased ATP generation in vitro in a DNP and oligomycin-sensitive manner. Conclusions : These results suggest that enhanced relocalization of dystrophin to the sarcolemma during reperfusion may be a mechanistic link between IPC-mediated improvement of mitochondrial function and its protection against oncosis upon reperfusion.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (8 results)

All 2006 2005 2004

All Journal Article (8 results)

  • [Journal Article] Dystrophin is a possible end-target of ischemic preconditioning against cardiomyocyte oncosis during the early phase of reperfusion.2006

    • Author(s)
      Kyoi S, Otani H, Hamano A, Matsuhisa S, Akita Y, Fujiwara H, Hattori R, Imaura H, Iwasaka T.
    • Journal Title

      Cardiovasc Res 70

      Pages: 354-363

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Dystrophin is a possible end-target of ischemic preconditioning against cardiomyocyte oncosis during the early phase of reperfusion.2006

    • Author(s)
      Kyoi S, Otani H, Hamano A, Matsuhisa S, Akita Y, Fujiwara H, Hattori R, Imamura H, Iwasaka T
    • Journal Title

      Cardiovasc Res 70

      Pages: 354-363

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.2005

    • Author(s)
      Sumida T, Otani H, Kyoi S, Okada T, Fujiwara H, Nakao Y, Kido M, Imamura H.
    • Journal Title

      American Journal of Physiology 288

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Integrated pharmacological preconditioning and Memory of cardioprotection : the role of protein kinase C and phosphatidylinositol 3-kinase.2005

    • Author(s)
      Okada T, Otani H, Wu Y, Uchiyama T, Kyoi S, Hattori R, Sumide T, Fujiwara H, Imamura H.
    • Journal Title

      American Journal of Physiology 289

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation.2005

    • Author(s)
      Okada T, Otani H, Wu Y, Kyoi S, Enoki C, Fujiwara H, Sumida T, Hattori R, Imamura H.
    • Journal Title

      American Journal of Physiology 289

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.2005

    • Author(s)
      Sumida T et al.
    • Journal Title

      American Journal of Physiology 288

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Integrated pharmacological preconditioning and memory of cardioprotection : the role of protein kinase C and phosphatidylinositol 3-kinase.2005

    • Author(s)
      Okada T et al.
    • Journal Title

      American Journal of Physiology 289

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Ischemic preconditioning-mediated restoration of membrane dystrophin during reperfusion correlates with protection against contraction-induced myocardial injury2004

    • Author(s)
      Kido M, Otani H, et al.
    • Journal Title

      Am J Physiol 287

    • Related Report
      2004 Annual Research Report

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Published: 2004-04-01   Modified: 2016-04-21  

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