1988 Fiscal Year Final Research Report Summary
CHANGE IN MYOSIN HEAVY CHAIN IN PULMONARY ARTERY-BANDED AND DEBANDED RAT HEART
| Project/Area Number |
62570442
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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 |
Pediatrics
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| Research Institution | HEART INSTITULE OF JAPAN, TOKYO WOMEN'S MEDICAL COLLEGE |
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Principal Investigator |
MATSUOKA Rumiko DEPT. OF PEDIATRIC CARDIOLOGY, HEART INSTITUTE OF JAPAN・RESEARCH ASSOCIATE, 循環器小児科, 助手 (50120051)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAO Atsuyoshi DEPT. OF PEDIATRIC CARDIOLOGY, HEART INSTITATE OF JAPAN・PROFESSOR (70075167)
IMAMURA Shin-ichiro RESEARCH DIVISION, HEART INSTITUTE OF JAPAN・RESEARCH ASSOCIATE (00176497)
KIMURA Misa DEPT. OF PEDIATRIC CARDIOLOGY, HEART INSTITUTE OF JAPAN・RESEARCH ASSOCIATE (60192019)
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| Project Period (FY) |
1987 – 1988
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| Keywords | CARDIAC MYOSIN / MYOSIN GENE / CONTRACTILE PROTEIN / 肺動脈絞扼 |
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| Research Abstract |
It has been shown that the distribution of cardiac myosin heavy chain (MHC) isozymes is regulated during development by hemodynamic change and hormonal stimuli and this transition is mainly regulated by pretranslational mechanisms. To study whether the changes in MHC gene expression produced by left-sided overload are limited to the left ventricle (LV) or extend to the right ventricle (RV), or whether right-sided overload are limited to RV or extends to LV, we examined the MHC gene expression and isozyme transition. For these studies, pulmonary artery-banded (PAB) rats and sham-operated rats were prepared. These data were compared with previous study on aortic coarctated (CoA) rats. Results : There was no significant differences of peak-systolic pressure, wall thickness, V3-MHC and -MHC in RV of the CoA rats and in LV of the PAB rats compared with shzm-operated rats, while significant induction of them in LV of the CoA rats and in the RV of PAB rats. These animals showed both ventricular end-diastolic pressure were within the normal range. Conclusions : We found that the changes in the MHC gene expression and isozyme produced by one-sided ventricular overload are limited to the involved ventricle and do not extend to the other one. In this study, it is suggested that MHC gene regulation during pressure overload may not be induced by intrinsic factors, such as hormone or catecholamine or ANP, but is induced by direct local response to increased load.
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