Aerobic Training-induced Upregulation of YAP1 and Prevention of Cardiac Pathological Hypertrophy in Male Rats

有氧训练诱导YAP1上调并预防雄性大鼠心脏病理性肥大

阅读:1

Abstract

BACKGROUND: Pathological hypertrophy is one of the negative consequences of cardiac sympathetic hyperactivity. Recent studies have shown that YAP1 plays a critical role in cardiomyocytes hypertrophy. Considering the preventive role of exercise training in cardiovascular diseases, the present study was conducted to examine the effect of aerobic exercise training on YAP1 gene expression and its upstream components. METHODS: Eighteen male Wistar rats were randomly divided into aerobic training and control groups. Aerobic training was performed one hour/day, five days per week, for eight weeks, on a treadmill at 65-75% VO(2) max. Pathological hypertrophy was induced by injecting 3 mg/kg(-1) of isoproterenol for seven days. The left ventricle was separated, and YAP1, 3-mercaptopyruvate sulfurtransferase (MST), large tumor suppressor (LATS), and mitogen-activated protein 4 kinase (MAP4K) gene expressions were assessed and YAP1 protein levels were also assessed by western blotting. Cell apoptosis was detected by TUNEL assays. The between-group differences were evaluated using the T-test and P value <0.05 was considered statistically significant. RESULTS: There were no significant between-group differences in MST gene expression (P = 0.061); meanwhile, in the training group, LATS and Map4K expressions were suppressed, followed by a significant increase in YAP1 expression (P < 0.001). Compared to the control group, the left ventricular weight increased significantly in the training group while the cardiomyocyte apoptosis decreased. CONCLUSIONS: The results showed that, by reducing LATS, aerobic training-induced YAP1 upregulation can help prevent the propagation of cardiomyocyte apoptosis due to pathological conditions.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。