Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Role of miR-134 in angiotensin II-induced vascular cell pathological changes in atherosclerosis

Jing Chen , Qi Hu, Bofang Zhang, Xiaopei Liu, Shuo Yang, Hong Jiang

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China;

For correspondence:- Jing Chen Email: chenjingjjx@163.com Tel:+278804191181046

Accepted: 23 April 2019 Published: 31 May 2019

Citation: Chen J, Hu Q, Zhang B, Liu X, Yang S, Jiang H. Role of miR-134 in angiotensin II-induced vascular cell pathological changes in atherosclerosis. Trop J Pharm Res 2019; 18(5):967-973 doi: 10.4314/tjpr.v18i5.9

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the role of miR-134 in vascular smooth muscle cell dysfunction-related cardiovascular disease.

Methods: The effect of miR-134 was evaluated after human aortic smooth muscle cells (HASMCs) were transfected with miR-134 mimics. The expression levels of p-Akt, mechanistic target of rapamycin (mTOR), cleaved caspase-3, p53, and β-actin were evaluated by immunoblotting. Terminal deoxynucleotidyl transferase dUTP nick-end labeling was used to measure cell apoptosis. Reactive oxygen species levels were assayed by @258;uorescence microscopy after staining with 2’,7’–dichlorofluorescein diacetate.

Results: Angiotensin II treatment induced miR-134 expression and Akt/mTOR activation, and inhibited cell viability in HASMCs (p < 0.01). Co-treatment with miRNA-134 reversed Ang II-induced HASMC dysfunction (p < 0.01). Overexpression of miR-134 is protective in Ang II-induced oxidative stress and apoptosis via the Akt/mTOR pathway (p < 0.05).

Conclusion: MicroRNA-134 in HASMCs is a potential therapeutic target for preventing Ang II-induced cardiac dysfunction via modulating Akt/mTOR pathway.

Keywords: MiR-134, Akt/mTOR pathway, Oxidative stress, HASMCs, Atherosclerosis