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Functional Study of Sarcoglycan in Cardiomyopathic Muscle Cells

Research Project

Project/Area Number 12670718
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionNational Cardiovascular Center Research Institute

Principal Investigator

IWATA Yuko  National Cardiovascular Center Research Institute Molecular Physiology Investigator, 循環分子生理部, 室員 (80171908)

Project Period (FY) 2000 – 2001
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Keywordscardiomyopathic hamster / apoptosis / Ca abnormality / Sarcoglycan / myotube / stretch-channel / ストレッチチャネル / 心筋症 / ジストロフィー / チャネル / Ca代謝
Research Abstract

Deficiency of delta-sarcoglycan, a component of the dystrophin-glycoprotein complex, causes cardiomyopathy and skeletal muscle dystrophy in BIO14.6 hamsters. Using cultured myotubes (for 2-4 days) prepared from muscle of normal and BIO14.6 hamsters (30-40 day old), we investigated the possibility that the delta-sarcoglycan in calcium metabolism which may ultimately leads to myocyte damage. Immunoblot analysis revealed that the contents of membrane proteins involved in cell Ca handling such as L-type Ca channel, ryanodine receptor, SR-CaATPase, Na/Ca exchanger were not different between control and BI014.6 myotubes. ^<45>Ca^<2+> influx into BIO14.6 myotubes 2+ under resting conditions was significantly higher (up to1.8-fold at 5 min) than in controls, suggesting that Ca^<2+> influx is activated in BIO 14.6 myotubes. When these cells were subjected to cyclic elongation of up to 20 % for 1h, a marked increase in creatine phosphokinase (CK) release into the medium was obsereved in only BIO14.6 myotubes. 100μM GdCl_3 reduced ^<45>Ca^<2+> influx and CK release. Transfection of delta sarcoglycan using 2+ adenovirus vector also rescue abnormal calcium metabolism and CK release The increased resting Ca influx in BIO14.6 myotubes may be due to the increased basal activity of stretch-activated cation channels detected in these myotubes and these results suggest a possible mechanism for cell damage in this animal model of muscular dystrophy.

Report

(3 results)
  • 2001 Annual Research Report   Final Research Report Summary
  • 2000 Annual Research Report
  • Research Products

    (15 results)

All Other

All Publications (15 results)

  • [Publications] Nakamura, T.Y., et al.: "Stretch-activated cation channels in skeletal muscle myotubes from sarcoglycan-deficient hamsters"Am.J.Physiol.Cell Physiol.. 281. C690-C699 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Sampaolesi, M.et al.: "Stretch-induced cell damage in sarcoglycan-deficient myotubes"Pflugers Archiv. 442. 161-170 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] 岩田 裕子: "アクチン結合タンパク質としてのシントロフィンの機能的役割"心筋の構造と代謝. 2000 23. 219-228 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Iwata, Y et al.: "Abnormal Calcium homeostasis and cell damage in dystrophic myotube"Journal of Molecular and Cellular Cardiology. 33. A51 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Katanosaka, Y., et al.: "Isolation and characterization of myotubes from BIO14.6 hamsters"Journal of Molecular and Cellular Cardiology. 33. A56 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Nakamura, T.Y., et al: "Stretch-activated cation channels in skeletal muscle myotubes from sarcoglycan-deficient hamsters"Am. J. Physiol. Cell Physiol.. 281. C690-699 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Sampaolsesi, M. et al: "Stretch-induced cell damage in sarcoglycan-deficient myotubes"Pfugers Archiv.. 442. 161-170 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Iwata, Y., et al: "Functional role of syntophin as an actin -binding protein"Cardiac structure and function. 23. 219-228 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Iwata, Y et al: "Abnormal Calcium homeostasis and cell damage in dystrophic myotubes"Journal of Molecular and Cellular Cardiology. 33. A51 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Katanosaka, Y., et al: "Isolation and characterizat in of myotubes from BIO14.6 hamsters"Journal of Molecular and Cellular Cardiology. 33. A56 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] 岩田 裕子: "Stretch-activated cation-permeable channels are activated in cultured myotubes from skeletal muscle of sarcoglycan deficient hamster"Am.J.Physiol.Cell Physiol.. 281. C690-C699 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] 岩田 裕子: "Stretch-induced cell damage in sarcoglycan-deficient myotubes"Pflugers Archiv. 442. 161-170 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] 岩田 裕子: "アクチン結合タンパク質としてのシントロフィンの機能的役割"心筋の構造と代謝. 2000 23. 219-228 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] 岩田裕子: "Stretch-activated cation-permeable channels are activated in cultured myotubes from skeletal muscle of sarcoglycan deficient hamster."Am.J.Phys.. (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] 岩田裕子: "Stretch-induced cell damage in sarcoglycan-deficient myotubes."Pflugers Archiv. (2001)

    • Related Report
      2000 Annual Research Report

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Published: 2000-04-01   Modified: 2016-04-21  

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