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Int. J. Mol. Sci. 2015, 16(7), 14511-14525; doi:10.3390/ijms160714511

MiR-21 Protected Cardiomyocytes against Doxorubicin-Induced Apoptosis by Targeting BTG2

1
Department of Pathology, the Second Xiangya Hospital, Central South University, Changsha 410000, Hunan, China
2
Department of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha 410000, Hunan, China
3
Food Science and Technology College, Hunan Agricultural University, Changsha 410000, Hunan, China
*
Authors to whom correspondence should be addressed.
Academic Editor: H. W. M. Niessen
Received: 13 April 2015 / Revised: 26 May 2015 / Accepted: 4 June 2015 / Published: 26 June 2015
(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure)
View Full-Text   |   Download PDF [2376 KB, uploaded 26 June 2015]   |  

Abstract

Doxorubicin (DOX) is an anthracycline drug with a wide spectrum of antineoplastic activities. However, it causes cardiac cytotoxicity, and this limits its clinical applications. MicroRNA-21 (miR-21) plays a vital role in regulating cell proliferation and apoptosis. While miR-21 is preferentially expressed in adult cardiomyocytes and involved in cardiac development and heart disease, little is known regarding its biological functions in responding to DOX-induced cardiac cytotoxicity. In this study, the effects of DOX on mouse cardiac function and the expression of miR-21 were examined in both mouse heart tissues and rat H9C2 cardiomyocytes. The results showed that the cardiac functions were more aggravated in chronic DOX injury mice compared with acute DOX-injury mice; DOX treatment significantly increased miR-21 expression in both mouse heart tissue and H9C2 cells. Over-expression of miR-21 attenuated DOX-induced apoptosis in cardiamyocytes whereas knocking down its expression increased DOX-induced apoptosis. These gain- and loss- of function experiments showed that B cell translocation gene 2 (BTG2) was a target of miR-21. The expression of BTG2 was significantly decreased both in myocardium and H9C2 cells treated with DOX. The present study has revealed that miR-21 protects mouse myocardium and H9C2 cells against DOX-induced cardiotoxicity probably by targeting BTG2. View Full-Text
Keywords: microRNA-21 (miR-21); doxorubicin (DOX); cardiotoxicity; B cell translocation gene 2 (BTG-2) microRNA-21 (miR-21); doxorubicin (DOX); cardiotoxicity; B cell translocation gene 2 (BTG-2)
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. (CC BY 4.0).

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MDPI and ACS Style

Tong, Z.; Jiang, B.; Wu, Y.; Liu, Y.; Li, Y.; Gao, M.; Jiang, Y.; Lv, Q.; Xiao, X. MiR-21 Protected Cardiomyocytes against Doxorubicin-Induced Apoptosis by Targeting BTG2. Int. J. Mol. Sci. 2015, 16, 14511-14525.

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