长链非编码 RNA XIST 通过介导 miR-150-5p/Bax 抑制急性心肌梗死缺氧诱导的心肌细胞凋亡。
LncRNA XIST inhibits hypoxia-induced cardiomyocyte apoptosis via mediating miR-150-5p/Bax in acute myocardial infarction.
机构信息
Department of Cardiovascular, Gansu Provincial Hospital of TCM, Lanzhou, P.R. China.
出版信息
Eur Rev Med Pharmacol Sci. 2020 Feb;24(3):1357-1366. doi: 10.26355/eurrev_202002_20193.
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.
目的
急性心肌梗死（AMI）可导致由缺氧引起的长期心肌缺血。长链非编码 RNA（lncRNA）影响心脏病的发生和发展。本研究探讨了 lncRNA X 失活特异性转录物（XIST）在缺氧诱导损伤的 H9c2 细胞中的作用和机制。
材料和方法
采用噻唑蓝（MTT）比色法、Transwell 实验和流式细胞术分别分析不同条件下 H9c2 细胞的存活、侵袭、迁移和凋亡情况。采用实时荧光定量聚合酶链反应（qRT-PCR）或 Western blot 检测相关基因的表达。
结果
XIST 在缺氧诱导损伤的 H9c2 细胞中过度表达，沉默 XIST 可减轻细胞损伤。XIST 的上调通过与 miR-150-5p 竞争结合促进 B 细胞淋巴瘤 2 相关 X（Bax）的表达。
结论
XIST 通过调节 miR-150-5p/Bax 轴保护心肌细胞免受缺氧诱导的损伤，提示 XIST 是 AMI 治疗的重要靶点。
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