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Connexin43 as a determinant of arrhythmia inducibility in cardiac gap junction of infarct heart

Research Project

Project/Area Number 14571286
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Thoracic surgery
Research InstitutionNippon Medical School

Principal Investigator

KANNO Shigeto  Nippon Medical School, Department of Surgery, Fellow, 医学部, 助手 (20291718)

Co-Investigator(Kenkyū-buntansha) OHMORI Hiroya  Nippon Medical School, Department of Surgery, Fellow, 医学部, 助手 (40343587)
MIYAGI Yasuo  Nippon Medical School, Department of Surgery, Fellow, 医学部, 助手 (00350611)
NITTA Takashi  Nippon Medical School, Department of Surgery, Assistant Professor, 医学部, 助教授 (40256954)
SASAKI Takashi  Nippon Medical School, Department of Surgery, Fellow, 医学部, 助手 (80350065)
清水 一雄  日本医科大学, 医学部, 教授 (20133449)
田中 茂夫  日本医科大学, 医学部, 教授 (70089720)
石井 庸介  日本医科大学, 医学部, 助手 (10307895)
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
KeywordsGap Junction / Connexin43 / Isohemia / Arrhythmia
Research Abstract

Sudden cardiac death is common in patients who have survived myocardial infarction (MI), but the molecular mechanisms responsible are complex and poorly defined. To facilitate development of a mouse model to define gene products critical in lethal arrhythmia following MI, we created MI by LAD coronary occlusion in C57BL/6J mice heterozygous for a major gap junction protein Cx43 null allele and wildtype. To characterize structural consequences in MI, we used echocardiography. Left ventricular end-diastolic volume was increased as a function of infarct size at both 1 and 10 weeks after surgery. However, no differences in the relationship between left ventricular end-diastolic volume and infarct size were seen in wildtype and Cx43-deficient mice. Post-infarction remodeling as a function of infarct size was not affected by diminished Cx43 expression. Isolated hearts with healed MI were analyzed with extrastimulus protocol for inducing ventricular tachycardia (VT). VT was induced in both Cx … More 43+/-and +/+ hearts with MI. Ventricular sections were examined histologically. Infarct size was smaller in Cx43+/-mice compared with +/+ mice. Specific morphological features were evaluated including whether infarcts were transmural or non-transmural, and the presence or absence of ventricular aneurysmal dilatation, patchy interstitial fibrosis at infarct border zones, and surviving subendocardial myocytes. A layer of surviving subendocardial myocytes was seen more frequently in hearts in which VT could be induced but the occurrence of this feature was similar in Cx43+/-and +/+ hearts. The other features of post-infarct remodeling pertinent to development of arrhythmias and contractile dysfunction in hearts with healed infarcts were also observed with equal frequency in Cx43 +/-and +/+ hearts. Reduced basal coupling does not by itself significantly alter infarct healing or post-MI remodeling. Analysis of arrhythmias following MI in mouse lines with defined genetic defects will shed light on the roles of these proteins in sudden cardiac death in patients with healed MI. Less

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] Shigeto Kanno et al.: "Echocardiographic evaluation of ventricular remodeling in a mouse model of myocardial infarction"J Am Soc of Echocardiogr. 15(6). 601-609 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Shigeto Kanno et al.: "Connexin43 as a determinant of myocardial infarct size following coronary occulusion in mice"J Am Coll of Cardiol. 41. 681-686 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Shigeto Kanno, Deborah L.Lerner, Richard B.Schuessler, Tetsuo Betsuyaku, Kathryn A.Yamada, Jeffrey E.Saffitz, Attila Kovacs: "Echocardiographic evaluation of ventricular remodeling in a mouse model of myocardial infarction"J Am Soc of Echocardiogr.. 15(6). 601-609 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Shigeto Kanno, Attila Kovacs, Kathryn A.Yamada, Jeffrey E.Saffitz: "Connexin43 as a determinant of myocardial infarct size following coronary occulusion in mice"Journal of the American College of Cardiology. 41. 681-686 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Shigeto Kanno: "Connexin43 as a determinantof myocardial infarct size following coronary occulusion in mice"Journal of the American College of Cardiology. 41. 681-686 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Shigeto Kanno: "The role of myocardial gap junctions in electrical conduction and arrhythmogenesis"Cardiovascular Pathology. 10. 169-177 (2001)

    • Related Report
      2002 Annual Research Report
  • [Publications] Shigeto Kanno: "Echocardiographic evaluation of ventricular remodeling in a mouse model of myocardial infarction"Journal of the American Society of Echocardiography. 15(6). 601-609 (2002)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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