MicroRNA-520d-3p alleviates hypoxia/reoxygenation-induced damage in human cardiomyocytes by targeting ATG-12
- PMID: 33389611
- DOI: 10.1007/s11239-020-02352-9
MicroRNA-520d-3p alleviates hypoxia/reoxygenation-induced damage in human cardiomyocytes by targeting ATG-12
Abstract
Hypoxia/reoxygenation (H/R) induced injury results in extensive damages to myocardial tissue in patients with coronary heart disease, which leads to heart failure. MicroRNA (miRNA) is thought to be associated with myocardial H/R injury. The purpose of this study was to investigate the in vitro role of microRNA-520d-3p in human myocardial cell (HCM) myocardial H/R injury. MTT method and Annexin V-FITC flow cytometry were employed to measure the viability and apoptosis of H/R treated HCM. RT-qPCR was employed to determine miRNA and mRNA expression. MicroRNA-520d-3p mimic and microRNA-520d-3p inhibitor were used to overexpression and inhibit the expression of microRNA-520d-3p. In addition, pcDNA3.1-ATG12 was used to upregulate ATG12 expression. The protein levels of ATG12, Bcl-2 and autophagy related-genes were determined by western blotting. Hypoxia/reoxygenation (H/R) injury could inhibit cell viability, apoptosis and inhibited microRNA-520d-3p expression in HCM. The down-regulation of microRNA-520d-3p inhibited cell viability and induced apoptosis in HCM. The overexpression of microRNA-520d-3p attenuated the effects of H/R treatment on the viability and apoptosis of HCM cells. In addition, microRNA-520d-3p inhibited the expression of autophagy-associated 12 (ATG12). More importantly, H/R treatment could promote autophagy in HCM, and microRNA-520d-3p mimic transfection could significantly reverse this effect. Our result indicated that overexpression of microRNA-520d-3p attenuated the effect of H/R treatments on cell viability, apoptosis and autophagy, through partly regulating ATG12 expression in HCM.
Keywords: ATG12; Autophagy; H/R injury; Heart failure; microRNA-520d-3p.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.
References
-
- Dong G, Chen T, Ren X, Zhang Z, Huang W, Liu L, Luo P, Zhou H (2016) Rg1 prevents myocardial hypoxia/reoxygenation injury by regulating mitochondrial dynamics imbalance via modulation of glutamate dehydrogenase and mitofusin 2. Mitochondrion 26:7–18 - DOI
-
- Kuo H-F, Liu P-L, Chong I-W, Liu Y-P, Chen Y-H, Ku P-M, Li C-Y, Chen H-H, Chiang H-C, Wang C-L (2016) Pigment epithelium-derived factor mediates autophagy and apoptosis in myocardial hypoxia/reoxygenation injury. PloS one 11(5):e0156059 - DOI
-
- Zhao Y-P, Wang F, Jiang W, Liu J, Liu B-L, Qi L-W, Zhou W (2019) A mitochondrion-targeting tanshinone IIA derivative attenuates myocardial hypoxia reoxygenation injury through a SDH-dependent antioxidant mechanism. J Drug Target 27(8):896–908 - DOI
-
- Cheng M-Y, Cheng Y-W, Yan J, Hu X-Q, Zhang H, Wang Z-R, Yin Q, Cheng W (2016) SIRT6 suppresses mitochondrial defects and cell death via the NF-κB pathway in myocardial hypoxia/reoxygenation induced injury. Am J Translat Res 8(11):5005
-
- Zhigang Y, Chen J, Jin L, Guo W, Juan W, Huang S (2018) GLP-1 agonist protects myocardial hypoxia-reoxygenation injury through PI3K/Akt signaling pathway: an experimental study. Chin J Endocrinol Metab 34(1):61–66
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