| Project/Area Number |
01570506
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kururme University |
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Principal Investigator |
ADACHI Kyo Kurume Univ., School of Med., Assoc. Prof., 医学部, 助教授 (30131741)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Kiichiro Kurume Univ., School of Med., Assist., 医学部, 助手 (00210526)
SAKANASHI Toshihiko (YAMAMOTO Kiichiro) Kurume Univ., School of Med., Assist., 医学部, 助手 (30196076)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1990: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1989: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Protein Kinase C / Protooncogene / Myocardial Hypertrophy / Immunohistochemistry / In Situ Hybridization / Idiopathic Cardiomyopathy / 特発生心筋症 |
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| Research Abstract |
Protein kinase C (PKC) has a central role in the control many cellular processes. Recently, a correlation between PKC and cardiac hypertrophy has been reported in cultured rat cardiocytes. The purpose of this study is to investigate the role of PKC in the human myocardium in idiopathic cardiomyopathy (ICM). The subjects include 16 patients with hypertrophic cardiomyopathy (HCM), 12 patients with dilated cardiomyopathy, and 5 individuals as the control group. Right-side endomyocardial biopsy specimens were obtained. The specimen was immediately frozen by liquid nitrogen for immunohistochemical procedures. A monoclonal anti-protein kinase C antibody (clone MC5, Amersham) was used for this study. Immunohistochemical reaction according to an indirect immunoperoxidase (avidin-biotin-peroxidase complex method) were performed with some modifications. The PKC was observed as a fine granular substances, which were located both in the cytoplasm and in the peripheral regions, but mainly in the cytoplasm. The incidence of patients with PKC-positive myocytes was more frequent in hypertrophic cardiomyopathy than in dilated cardiomyopathy. The intensity of immunoreactivity of PKC in the cytoplasm of the myocytes was stronger in hypertrophic cardiomyopathy than in dilated cardiomyopathy. Thus, it is suggested that PKC may play an important role in the pathogenesis of abnormal myocardial hypertrophy in cardiomyopathy.
Expression of protooncogenes (c-myc, c-fos, c-Ha-ras) in myocardium in patients with cardiomyopathy were all negative in spite of our expectation. Further experiments will be necessary to get good results.
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