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
Int. J. Mol. Sci. 2015, 16(7), 14511-14525; https://doi.org/10.3390/ijms160714511
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)
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.
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Keywords:
microRNA-21 (miR-21); doxorubicin (DOX); cardiotoxicity; B cell translocation gene 2 (BTG-2)
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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.
AMA 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. International Journal of Molecular Sciences. 2015; 16(7):14511-14525.
Chicago/Turabian StyleTong, Zhongyi; Jiang, Bimei; Wu, Yanyang; Liu, Yanjuan; Li, Yuanbin; Gao, Min; Jiang, Yu; Lv, Qinglan; Xiao, Xianzhong. 2015. "MiR-21 Protected Cardiomyocytes against Doxorubicin-Induced Apoptosis by Targeting BTG2" Int. J. Mol. Sci. 16, no. 7: 14511-14525.
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