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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 960362, 16 pages
http://dx.doi.org/10.1155/2014/960362
Research Article

Effects of Downregulation of MicroRNA-181a on H2O2-Induced H9c2 Cell Apoptosis via the Mitochondrial Apoptotic Pathway

Lei Wang,1,2 He Huang,1,2 Yang Fan,1,2 Bin Kong,1,2 He Hu,1,2 Ke Hu,1,2 Jun Guo,1,2 Yang Mei,1,2 and Wan-Li Liu1,2

1Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Jiefang Road 238, Wuhan 430060, China

Received 27 October 2013; Revised 16 December 2013; Accepted 19 December 2013; Published 11 February 2014

Academic Editor: Neelam Khaper

Copyright © 2014 Lei Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Glutathione peroxidase-1 (GPx1) is a pivotal intracellular antioxidant enzyme that enzymatically reduces hydrogen peroxide to water to limit its harmful effects. This study aims to identify a microRNA (miRNA) that targets GPx1 to maintain redox homeostasis. Dual luciferase assays combined with mutational analysis and immunoblotting were used to validate the bioinformatically predicted miRNAs. We sought to select miRNAs that were responsive to oxidative stress induced by hydrogen peroxide (H2O2) in the H9c2 rat cardiomyocyte cell line. Quantitative real-time PCR (qPCR) demonstrated that the expression of miR-181a in H2O2-treated H9c2 cells was markedly upregulated. The downregulation of miR-181a significantly inhibited H2O2-induced cellular apoptosis, ROS production, the increase in malondialdehyde (MDA) levels, the disruption of mitochondrial structure, and the activation of key signaling proteins in the mitochondrial apoptotic pathway. Our results suggest that miR-181a plays an important role in regulating the mitochondrial apoptotic pathway in cardiomyocytes challenged with oxidative stress. MiR-181a may represent a potential therapeutic target for the treatment of oxidative stress-associated cardiovascular diseases.