2002 Fiscal Year Final Research Report Summary
A study on the mechanism of myocardial injury in myocarditis and dilated cardiomyopathy.
| Project/Area Number |
11670714
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
NISHIKAWA Toshio Tokyo Women's Medical University, Associate Professor, 医学部, 助教授 (50120019)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIYAMA Shigeru Tokyo Women's Medical University, Assistant, 医学部, 助手 (20297542)
MASUDA Akihiro Tokyo Women's Medical University, Associate Professor, 医学部, 助教授 (60209434)
KASAJIMA Takeshi Tokyo Women's Medical University, Professor, 医学部, 教授 (30045653)
HIROE Michiaki Tokyo Medical Dental University, Instructor, 医学部, 講師 (80101872)
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| Project Period (FY) |
1999 – 2002
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| Keywords | Dilated cardiomyopathy / chronic myocarditis / rat / tissue injury / infiltrated lymphocyte / apoptosis / Fas / Fas ligand system |
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| Research Abstract |
It has generally been recognized that myocarditis may be implicated in the pathogenesis of dilated cardiomyopathy. However, the mechanism of myocardial damage in the chronic stage of myocarditis is still unclear. In this study myocarditis was induced in Lewis rats by injection of porcine cardiac myosin and rats were harvested on day 21 or 74 after the initial injection. Apoptotic cell death was confirmed by in situ nick end labeling assay and gel-electrophoresis for DNA fragmentation on day 21, but none was disclosed on day 74. The expression of Fas mRNA and protein was detected on day 21 in the myocardium. In addition, Fas ligand was detected in some infiltrating lymphocytes. Some rats were injected with anti-Fas antibody or anti-Fas ligand antibody, and subsequently, myocardial damage was less severe than that in untreated rats on day 74. These results suggested that inhibition of apoptotic phenomenon in the acute stage may be related to the reduction of myocardial damage in the chronic stage of myocarditis.
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