The role of miR-711 in cardiac cells in response to oxidative stress and its biogenesis: a study on H9C2 cells

作者：Duo Zhao, Hao Zheng, Adam Greasley, Fengjun Ling, Qinfeng Zhou, Bowen Wang, Tiffany Ni, Ishita Topiwala, Cuilin Zhu, Tina Mele, Kexiang Liu, Xiufen Zheng · 发表于：Cellular & Molecular Biology Letters · 年份：2020 · DOI：10.1186/s11658-020-00206-z · 被引用次数：13 · 研究领域：MicroRNA in disease regulation、Fibroblast Growth Factor Research、Hydrogen's biological and therapeutic effects

BACKGROUND: Oxidative stress results in cell apoptosis/death and plays a detrimental role in disease development and progression. Stressors alter the miRNA expression profile and miRNAs play a role in the cell response to stress. We previously showed that miR-711 is significantly over-expressed in extended cold ischemia reperfusion injured hearts in heart transplant. In this study, we aimed to investigate the role of miR-711 in cardiac cell damage in response to oxidative stress and how miR-711 is regulated. METHODS: , or cold hypoxia/reoxygenation (H/R)) in vitro. H9c2 cells were transfected with miR-711 mimics, miR-711 inhibitors, or small interference RNA, using transfection reagents. The expression of miR-711 was measured by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell apoptosis/death was detected by flow cytometry and an IncuCyte system. Mitochondrial damage was detected by measuring the mitochondria membrane potential by flow cytometry. Gene expression was detected by qRT-PCR at the mRNA level and Western blotting and immunocytochemistry staining at the protein level. RESULTS: , and cold H/R. Over-expression of miR-711 increased cell apoptosis/death induced by AA and H/R whereas cell death was reduced by miR-711 inhibitors. MiR-711 induced cell death through negative regulation of angiopoietin 1 (Ang-1), fibroblast growth factor 14 (FGF14) and calcium voltage-gated channel subunit alpha1C (Cacna1c) genes. Both knockdown of hypoxia inducib...