MicroRNA-210 alleviates oxidative stress-associated cardiomyocyte apoptosis by regulating BNIP3. Issue 9 (2nd September 2017)

• Record Type: Journal Article
• Authors: Diao, Hongying; Liu, Bin; Shi, Yongfeng; Song, Chunli; Guo, Ziyuan; Liu, Ning; Song, Xianjing; Lu, Yang; Lin, Xiaoye; Li, Zhuoran
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 81:Issue 9(2017)
• Page Start: 1712
• Page End: 1720
• Publication Date: 2017-09-02
• Subjects: Bcl-2 adenovirus E1B 19kDa-interacting protein 3 -- ischemia/reperfusion -- miR-210 -- myocardial apoptosis -- oxidative stress; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2017.1343118
• Languages: English
• ISSNs: 0916-8451

Abstract

Abstract: Oxidative stress-induced myocardial apoptosis and necrosis are involved in ischemia/reperfusion (I/R) injury. This study was performed to investigate microRNA (miR)-210's role in oxidative stress-related myocardial damage. The expression of miR-210 was upregulated in myocardial tissues of I/R rats, while that of Bcl-2 adenovirus E1B 19kDa-interacting protein 3 (BNIP3) was downregulated. To simulate in vivo oxidative stress, H9c2 cells were treated with H2 O2 for 48 h. MiR-210 level was increased upon H2 O2 stimulation, peaked at 8 h, and then decreased. An opposite expression pattern of BNIP3 was observed. BNIP3 was demonstrated as a direct target of miR-210 via luciferase reporter assay. H2 O2 -induced cell apoptosis was attenuated by miR-210 mimics, whereas aggravated by miR-210 inhibitor. MiR-210 knockdown-induced cell apoptosis in presence of H2 O2 was attenuated by BNIP3 siRNA. Our work demonstrates that miR-210 plays a protective role in H2 O2 -induced cardiomyocyte apoptosis at least by regulating the pro-apoptotic BNIP3. Abstract: : MiR-210 targeted 3'-UTR and CDS of BNIP3 mRNA in H9c2 cells (A). The miR-210 knockdown-induced apoptosis was attenuated by BNIP3 siRNA (B).