miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase
Bo Long1, Tian-Yi Gan2, Rong-Cheng Zhang2,*, and Yu-Hui Zhang2,*
1Central Research Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union
Medical College, Beijing 100730, China, 2State Key Laboratory of Cardiovascular Disease, Heart Failure center, Fuwai Hospital,
National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing
100037, China
*Correspondence: zhangyhfw@163.com (YHZ); zhangrcfw@126.com (RCZ)
Received January 18, 2017; Revised June 22, 2017; Accepted June 25, 2017.; Published online July 31, 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/).
Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.
Keywords: apoptosis, hydrogen peroxide, ischemia/reperfusion, miR-23a, MnSOD

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31 July 2017 Volume 40,
Number 7, pp. 441~522

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