Dissociation of left ventricular hypertrophy, beta-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosis.
Dissociation of left ventricular hypertrophy, beta-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosis.
复制标题
升主动脉狭窄后大鼠左心室肥厚、β-肌球蛋白重链基因表达和肌球蛋白亚型转换的分离。
DOI：
10.1161/01.cir.95.5.1253
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发表时间：
1997
期刊：
影响因子：
37.8
通讯作者：
Rüegg,JC
中科院分区：
文献类型：
--
作者：
Wiesner,RJ;Ehmke,H;Faulhaber,J;Zak,R;Rüegg,JC
背景研究发现，胎儿β-肌球蛋白重链（β-MHC）基因的重新表达是大鼠表型重编程和心肌肥厚的标志。最近的体外研究强烈建议的作用，血管紧张素II的表型重编程。在目前的调查中，β-MHC基因的表达进行了研究，在压力超负荷肥大的实验模型，是不与并行激活的循环肾素-血管紧张素system.Methods和ResultsHypertrophy诱导大鼠升主动脉结扎（n=40）。7天后，肌球蛋白中β-MHC亚型的含量为31%（P<0.05），而假手术组低于5%。而在环志动物中，β-MHCmRNA水平没有特异性升高。而腹主动脉缩窄大鼠心脏β-MHCmRNA水平显著升高（3 ~ 5倍，P<0.05）。与假手术动物相比，左心室重量和左心室收缩压峰值均显著升高（腹主动脉缩窄术，+13%和164±7 mm Hg;升主动脉缩窄术，+27%和191±9 mm Hg）。血浆肾素活性升高大鼠腹主动脉束带（2.5倍，P<0.05），但不是在大鼠升主动脉banding.ConclusionsThe目前的工作结果不支持的概念，增加β-MHC基因表达是一个普遍的“稳定的晚期标记”的心肌肥厚大鼠。我们的研究结果表明，肾素-血管紧张素系统的刺激是至关重要的β-MHC基因的激活。
BackgroundReexpression of the fetal β-myosin heavy chain (β-MHC) gene was reported to be a marker for phenotypic reprogramming and cardiac hypertrophy in rats. Recent in vitro studies strongly suggested a role of angiotensin II for phenotypic reprogramming. In the present investigation, β-MHC gene expression was studied in an experimental model of pressure-overload hypertrophy that is not associated with a concurrent activation of the circulating renin-angiotensin system.Methods and ResultsHypertrophy was induced in rats by ascending aortic banding (n=40). After 7 days, myosin contained 31% (P<.05) of the β-MHC isoform in banded but <5% in sham-operated animals. However, no specific elevation of β-MHC mRNA levels was found in banded animals. In contrast, hearts of rats with abdominal aortic banding displayed a marked increase in β-MHC mRNA levels (3-fold to 5-fold,P<.05). Both the left ventricular weight and left ventricular peak systolic pressure were significantly elevated compared with sham-operated animals (abdominal aortic banding, +13% and 164±7 mm Hg; ascending aortic banding, +27% and 191±9 mm Hg). Plasma renin activity was elevated in rats with abdominal aortic banding (2.5-fold,P<.05) but not in rats with ascending aortic banding.ConclusionsThe results of the present work do not support the concept that increased β-MHC gene expression is a general “stable late marker” of myocardial hypertrophy in rats. Our results suggest that the stimulation of the renin-angiotensin system is crucial for the activation of the β-MHC gene.