微小RNA-30a在血管紧张素II诱导的心肌细胞自噬中的作用
Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II.
作者信息
Huang Jionghua, Huang Chunlin, Luo Yishan, Liu Shiming, Chen Ximing
机构信息
Department of Cardiology, the Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Department of Cardiology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China.
出版信息
J Renin Angiotensin Aldosterone Syst. 2015 Mar;16(1):1-5. doi: 10.1177/1470320314562060. Epub 2014 Dec 12.
OBJECTIVE
The aim of this study was to investigate whether MiR-30a regulates autophagy by regulating the Beclin-1 protein, which is the marker for autophagosomes during myocardial injury, when induced by angiotensin II (Ang II).
METHODS
We randomly assigned 20 rats into two equal groups: Control group and Ang II group. We detected the expression of MiR-30a by quantitative real-time polymerase chain reaction (RT-PCR), and we employed western blotting to detect the protein expression of Beclin-1.
RESULTS
In this study, we found that Ang II induced cardiomyocyte autophagy, together with down-regulation of MiR-30a and upregulation of the Beclin-1 protein. We also found that the Beclin-1 protein is regulated by MiR-30a, by transferring a MiR-30a mimic or AMO-204 into the cardiomyocytes.
CONCLUSION
These studies provided evidence that MiR-30a plays an important role in regulating autophagy through the Beclin-1 protein, during myocardial injury induced by Ang II.
目的
本研究旨在探讨在血管紧张素II（Ang II）诱导心肌损伤时，微小RNA-30a（MiR-30a）是否通过调控自噬体标记物Beclin-1蛋白来调节自噬。
方法
将20只大鼠随机分为两组，每组10只：对照组和Ang II组。采用定量实时聚合酶链反应（RT-PCR）检测MiR-30a的表达，并用蛋白质免疫印迹法检测Beclin-1蛋白的表达。
结果
在本研究中，我们发现Ang II诱导心肌细胞自噬，同时MiR-30a表达下调，Beclin-1蛋白表达上调。我们还发现，通过将MiR-30a模拟物或AMO-204转入心肌细胞，Beclin-1蛋白受MiR-30a调控。
结论
这些研究提供了证据，表明在Ang II诱导的心肌损伤过程中，MiR-30a通过Beclin-1蛋白在调节自噬中发挥重要作用。
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