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- Title
MicroRNA-210 alleviates oxidative stress-associated cardiomyocyte apoptosis by regulating BNIP3.
- Authors
Diao, Hongying; Liu, Bin; Shi, Yongfeng; Song, Chunli; Guo, Ziyuan; Liu, Ning; Song, Xianjing; Lu, Yang; Lin, Xiaoye; Li, Zhuoran
- 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 simulatein vivooxidative stress, H9c2 cells were treated with H2O2for 48 h. MiR-210 level was increased upon H2O2stimulation, 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. H2O2-induced cell apoptosis was attenuated by miR-210 mimics, whereas aggravated by miR-210 inhibitor. MiR-210 knockdown-induced cell apoptosis in presence of H2O2was attenuated by BNIP3 siRNA. Our work demonstrates that miR-210 plays a protective role in H2O2-induced cardiomyocyte apoptosis at least by regulating the pro-apoptotic BNIP3. 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).
- Subjects
MICRORNA; NON-coding RNA; MYOCARDIAL infarction
- Publication
Bioscience, Biotechnology & Biochemistry, 2017, Vol 81, Issue 9, p1712
- ISSN
0916-8451
- Publication type
Article
- DOI
10.1080/09168451.2017.1343118