| Project/Area Number |
02670409
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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 | The Jikei University School of Medicine |
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Principal Investigator |
NAGANO Makoto The Jikei University School of Medicine, Professor, 医学部, 教授 (60056497)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Mitsutoshi The Jikei University School of Medicine, Assistant, 医学部, 助手 (60177475)
TAKEDA Nobuakira The Jikei University School of Medicine, Lecturer, 医学部, 講師 (60112835)
高橋 薫 東京慈恵会医科大学, 医学部, 講師 (40112833)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | cardiac growth factor / cardiac chalone / angiotensin / Goldblatt hypertension rat / Cardiac hypertrophy / Cell culture / AngiotensinII / BrDu / DNA G_1 / DNA G_2 / embryonic chicken heart |
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| Research Abstract |
1)This study was taken to verify the role of cardiac growth factor in the hypertrophied heart and cardiac inhibiting factors in the normal rat heart. For this propose the hypertrophied hearts of Goldblatt hypertension type I and II rats and those of normal rats were used. The supernatants of homogenized heart muscles were chromatographied using a HPLC method. We examined the cardiac growth and inhibiting effects of the isolated fractions with cultured chicken embryonic cardiac myocytes. Simultaneously, the cardiac cell cycle of the hypertrophid rat heart was examined by DNA analysis with the flow cytometric method. If the hearts were overloaded due to hypertension, the growth of cardiac size could be induced by increased level of protein with a molecular weight 43 KD with isoelectric point 8.3 and by a decreased level of polyclonal proteins with isoelectric point 7.0-7.1. The proto-oncogenes appeared in early stage after cardiac overload. DNA change, by flow cytometric method, G2, M and S phase of the cardiac cell cycle increased later than proto-oncogenes. The appearances of the cardiac growth factor and the decrease of the cardiac chalones in the hypertrophied hearts occurred much later than the flow cytometric DNA changes. The maximum level of cardiac growth factor and the minimum level of cardiac chalone could be proved at 5-6 weeks after beginning of the cardiac overload.
2)This study was taken to verify the growth effect of Angiotensin II on the cultured cardiac myocytes. The effect of angiotensin II was estamated by comparing cell number, DNA content and cell volume of myocytes in the presence or absence of angiotensin II in cultured medium. The cell number increased dose dependently by angiotensin II. DNA analysis by flow cytometry revealed increased in S, G2 and M phase of the cell cycle. An immunohistochemical study using antibody to bromodeoxyuridine showed that DNA synthesis in chicken embryonic cardiac myocytes were markedly increased by angiotensin II.
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