LncRNA XIST inhibits hypoxia-induced cardiomyocyte apoptosis via mediating miR-150-5p/Bax in acute myocardial infarction.
Jian Zhou, Li D, Yang Bp, Cui Wj
Abstract
OBJECTIVE: Acute myocardial infarction (AMI) contributes to long-term cardiac ischemia induced by hypoxia. Long non-coding RNAs (lncRNAs) affect the development and progression of heart diseases. This study explored the role and mechanism of lncRNA X inactive specific transcript (XIST) in H9c2 cells with hypoxia-induced injury. MATERIALS AND METHODS: Methyl-thiazolyl-tetrazolium (MTT), transwell, and flow cytometry assays were employed to analyze the survival, invasion, migration, and apoptosis of H9c2 cells under different conditions, respectively. Expression of related genes was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) or Western blot. RESULTS: XIST was over-expressed in H9c2 cells with hypoxia-induced injury, and the silence of XIST alleviated cell injury. Up-regulation of XIST promoted the expression of B-cell lymphoma 2-Associated X (Bax) through competitive binding to miR-150-5p. CONCLUSIONS: XIST protects cardiomyocytes from hypoxia-induced injury by mediating miR-150-5p/Bax axis, suggesting that XIST is an important target for AMI treatment.