| Project/Area Number |
13670758
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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 | Osaka Medical College |
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Principal Investigator |
UKIMURA Akira Osaka Medical College Faculty of Medicine Research Associate, 医学部, 助手 (50257862)
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| Co-Investigator(Kenkyū-buntansha) |
KITAURA Yasushi Osaka Medical College Faculty of Medicine Professor, 医学部, 教授 (50084950)
DEGUCHI Hirofumi Osaka Medical College Faculty of Medicine Assistant Professor, 医学部, 助教授 (90131341)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Dilated vardiomyopathy / dystropin / enterovirus / protease 2A / cytokine |
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| Research Abstract |
Enteroviruses have been implicated in the pathogenesis of idiopathic dilated cardiomyopathy, however the mechanisms of this pathology is unknown. It is reported that coxsackievirus protease 2A cleaves dystrophin. There is increasing evidence that inflammatory cytokines play an important role in the development of heart failure. To evaluate the pathological role of coxsackievirus in DCM, we analyzed the degeration of dystrophin by western blot of dystrophin, and the relative quantity of cytokine mRNA expression in hearts from DCM patients by quantitative PCR. We used heart tissues resected from DCM patients at the time of elective partial ventriculectomy (PLV). We tried to amplify the full-length enterovirus gebome from the hearts of DCM patients to analyze the mutation of enterovirus genome.
it was not clear whether enterovirus in hearts of DCM patients cleaves dystropin by western blot analysis. We succeeded 31 end-long-length PCR(4kb) of enterovirus cDNA which codes protease 2A from the heart of a DCM patient. The number of IL-10-positive DCM cases was significantly smaller than normal controls (p=0.0036). One (10%) of ten DCM patients with IL-10 mRNA expression died after PLV, and ten (45%) of twenty-two DCM patients without IL-10 mRNA expression died. We suggest that patients with heart failure deteriorate in DCM cases without IL-10 mRNA expression in the myocardium.
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