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Myocardial protection during heart surgery by IGF-1 and bcl-2 gene introduction.

Research Project

Project/Area Number 10671275
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, School of medicine, assistant professor, 医学部, 講師 (60168979)

Co-Investigator(Kenkyū-buntansha) OSAKO Motohiko  Kansai Medical University, School of medicine, research associate, 医学部, 助手 (90223784)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
Keywordsmyocardial ischemia / IGF-1 / Bcl-xL / Bax / Bcl-2 / IGF-I
Research Abstract

Insulin like growth factor-1 (IGF-1) has become a promising tool for treatment with end-stage heart failure. Although the underlying mechanism for myocardial protection remains elusive, recent studies suggest that altered regulation of Bcl-2 family proteins may be involved in the cytoprotective action of IGF-1. It has also been clear that intracellular localization of Bcl-2 family proteins is crucial in regulating the release of death-promoting cytochrome c from mitochondria. Therefore, we have investigated the effect of IGF-1 on Bcl-2 family protein expression and cytochrome c release in isolated rat heart mitochondria. Rats were treated with intra-peritoneal injection with IGF-1(3mg/kg). Mitochondria were isolated from the heart 12, 24, and 36 hours after the treatment. Western blot analysis showed that Bcl-xL expression was maximally increased in the rat heart mitochondria 24 hours after IGF-1 treatment, while Bax expression was maximally down-regulated in the same mitochondrial fra … More ction. Neither Bcl-xL nor Bax protein was detected in the cytosol fraction at any time point after IGF-1treatment. Bcl-2 protein was undetectable in mitochondria, cytosol, microsome or nuclearmyofibrillar fraction. Immunohistochemical staining revealed that IGF-1-induced overexpression of Bcl-xL in the heart was confined to cardiomyocytes. Isolated rat heart mitochondria did not release cytochrome c without a respiratory substrate succinate even in the presence of 10μM CaィイD12+ィエD1. However, respiring mitochondria released cytochrome c in a CaィイD12+ィエD1 dependent manner. Cytochrome c release was attenuated in mitochondria obtained from the heart treated with IGF-1. These results suggest that IGF-1 differentially regulates expression of Bcl-xL and Bax proteins in the rat heart mitochondria. IGF-1-Induced inhibition of cytochrome c release from the mitochondria may represent a mechanism for inhibition of apoptotic cardimyocyte cell death in patients with end-stage heart failure, or with reperfusion injury. Less

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] Otani, H et al.: "Insulin-like growth factor-I improves recovery of cardiac performance during reperfusion in isolated rat heart by a Wortmannin-sensitive mechanism"JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. 35 : (2). 275-281 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Otani, H et al.: "Insulin-like growth factor-I improves recovery of cardiac performance during reperfusion in isolated rat heart by a Wortmannin-sensitive mechanism"JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. 35 : (2). 275-281 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Otani,H et. al: "Insulin-like growth factor-I improves recovery of cardiac performance during reperfusion in isolated rat heart by a Wortmannin-sensitive mechanism"JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. 35:(2). 275-281 (2000)

    • Related Report
      1999 Annual Research Report

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Published: 1998-04-01   Modified: 2016-04-21  

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