Mol. Cells 2017; 40(12): 916~924  https://doi.org/10.14348/molcells.2017.0164
MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β
Changlin Zhai1,2,3, Qang Qian2,3, Guanmin Tang2, Bingjiang Han2, Huilin Hu2, Dong Yin2, Haihua Pan2,
and Song Zhang1,*
1Department of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, 1665# Kongjiang
Road, Yangpu district, Shanghai 200092, P.R. China, 2Department of Cardiovascular Diseases, The Frist Affiliated Hospital of
Jiaxing University, Jiaxing 314000, P.R China, 3These authors contributed equally to this work.
*Correspondence: zhangsong3961@xinhuamed.com.cn
Received August 15, 2017; Revised October 23, 2017; Accepted October 26, 2017.; Published online December 14, 2017.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit (http://creativecommons.org/licenses/by-nc-sa/3.0/).
ABSTRACT
MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently unclear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expression level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that Gadd45β (growth arrest DNA damage-inducible gene 45β) was a direct target gene of miR- 206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of Gadd45β. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting Gadd45β.
Keywords:
apoptosis, cardiomyocyte, Gadd45β, ischaemia–reperfusion, miR-206


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