MicroRNA‐214 Protects Cardiac Myocytes Against H 2 O 2 ‐Induced Injury

• Published in: Journal of cellular biochemistry Vol. 115; no. 1; pp. 93 - 101
• Main Authors: Lv, Guangwei, Shao, Suxia, Dong, Hua, Bian, Xiaohua, Yang, Xingwei, Dong, Shimin
• Format: Journal Article
• Language: English
• Published: 01.01.2014
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.24636

ABSTRACT Reactive oxygen species (ROS)‐induced cardiac myocyte injury resulting from changes in the expression levels of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. The purpose of this study was to determine the potential roles of microRNA‐214 (miR‐214) in hydrogen peroxide (H 2 O 2 )‐mediated gene regulation in cardiac myocytes. In this study, we used quantitative real‐time RT‐PCR (qRT‐PCR) to demonstrate that miR‐214 was upregulated in cardiac myocytes after treatment with H 2 O 2 . We transfected cells with pre‐miR‐214 to upregulate miR‐214 expression and transfected cells with a miR‐214 inhibitor (anti‐miR‐214) to downregulate miR‐214 expression. H 2 O 2 ‐induced cardiac cell apoptosis was detected by flow cytometry. The level of apoptosis was increased by the miR‐214 inhibitor and decreased by pre‐miR‐214. Therefore, we believe that miR‐214 plays a positive role in H 2 O 2 ‐induced cardiac cell apoptosis. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is constitutively active and is considered to be the primary downregulator of the pro‐oncogenic PI3K/Akt pathway. Western blot analysis revealed that the expression of the PTEN protein in cardiac myocytes decreased after H 2 O 2 induction. Anti‐miR‐214 increased PTEN protein expression level, in contrast, pre‐miR‐214 decreased the PTEN protein expression level in cultured cardiac myocytes. These results indicate that PTEN is regulated by miR‐214 and serves as an important target of miR‐214 in cardiac myocytes. In conclusion, miR‐214 is sensitive to H 2 O 2 stimulation, and miR‐214 protects cardiac myocytes against H 2 O 2 ‐induced injury via one of its targets, PTEN. J. Cell. Biochem. 115: 93–101, 2014. © 2013 Wiley Periodicals, Inc.