CHANGE IN MYOSIN HEAVY CHAIN IN PULMONARY ARTERY-BANDED AND DEBANDED RAT HEART

肺动脉带状和去带状大鼠心脏肌球蛋白重链的变化

基本信息

批准号：
62570442
负责人：
MATSUOKA Rumiko
金额：
$ 1.28万
依托单位：
HEART INSTITULE OF JAPAN, TOKYO WOMEN'S MEDICAL COLLEGE
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-62570442/
关键词：
CARDIAC MYOSIN MYOSIN GENE CONTRACTILE PROTEIN 肺動脈絞扼

项目摘要

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.

已经表明，在发育过程中，通过血流动力学变化和激素刺激调节心脏肌球蛋白重链（MHC）同工酶的分布主要受转换机制调节。为了研究左侧超负荷产生的MHC基因表达的变化是否仅限于左心室（LV）或延伸至右心室（RV），还是右侧过载限于RV或延伸至LV，我们检查了MHC基因表达和同学转变。对于这些研究，制备了肺动脉带（PAB）大鼠和假手术大鼠。将这些数据与先前关于骨质（COA）大鼠的研究的研究进行了比较。结果：与SHZM锻造大鼠相比，COA大鼠的RV和PAB大鼠的LV中没有显着差异，而在COA大鼠的LV和PAB大鼠的RV中，PAB大鼠的LV没有显着差异。这些动物表现出室末端压力均在正常范围内。结论：我们发现，单方面心室超负荷产生的MHC基因表达和同工酶的变化仅限于所涉及的心室，并且不会延伸到另一个。在这项研究中，建议在压力超负荷期间的MHC基因调节可能不会由固有因素（例如激素，儿茶酚胺或ANP）诱导，而是通过直接局部对负载增加的局部反应引起的。