Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II. (March 2015)

• Record Type: Journal Article
• Authors: Huang, Jionghua; Huang, Chunlin; Luo, Yishan; Liu, Shiming; Chen, Ximing
• Is Part Of: Journal of the renin-angiotensin-aldosterone system. Volume 16:Number 1(2015:Mar.)
• Page Start: 1
• Page End: 5
• Publication Date: 2015-03
• Subjects: Animal study -- Beclin-1 -- angiotensin II -- autophagosome -- autophagy -- cardiomyocytes -- injury -- MiR-30a -- myocardial injury -- protein regulation -- rats; Renin-angiotensin system -- Periodicals; 616.132
• DOI: 10.1177/1470320314562060
• Languages: English
• ISSNs: 1470-3203

Abstract

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.