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首页> 外文期刊>Journal of biochemical and molecular toxicology >miR‐192‐5p mediates hypoxia/reoxygenation‐induced apoptosis in H9c2 cardiomyocytes via targeting of FABP3
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miR‐192‐5p mediates hypoxia/reoxygenation‐induced apoptosis in H9c2 cardiomyocytes via targeting of FABP3

机译：MiR-192-5P通过靶向Fabp3介导H9C2心肌细胞中的缺氧/雷诺化诱导的细胞凋亡

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Abstract Myocardial ischemia/reperfusion (I/R) injury is a leading cause of morbidity and mortality. In this study, we investigated the role of miR‐192‐5p in hypoxia/reoxygenation (H/R)‐induced cardiomyocyte apoptosis. H9c2 cardiomyocytes were subjected to H/R and tested for miR‐192‐5p expression. Overexpression and knockdown experiments were performed to determine the effects of manipulating miR‐192‐5p on apoptotic responses. H/R‐treated H9c2 cells exhibited a 2.2‐fold increase in miR‐192‐5p levels. Overexpression of miR‐192‐5p significantly augmented apoptosis in H9c2 cells after H/R, which was accompanied by a significant increase in the ratio of Bax/Bcl‐2. In contrast, delivery of anti‐miR‐192‐5p inhibitors significantly reduced apoptosis induced by H/R. FABP3 was identified to be a functional target of miR‐192‐5p. Restoration of FABP3 prevented apoptosis in miR‐192‐5p‐transfected H9c2 cells, whereas downregulation of FABP3 enhanced apoptosis in H/R‐exposed H9c2 cells. In conclusion, miR‐192‐5p mediates H/R‐induced apoptosis in cardiomyocytes by targeting FABP3 and represents a potential target for prevention of myocardial I/R injury.
机译：摘要心肌缺血/再灌注（I / R）损伤是发病率和死亡率的主要原因。在这项研究中，我们研究了MIR-192-5P在缺氧/雷诺（H / R）诱导的心肌细胞凋亡中的作用。 H9C2心肌细胞进行H / R并测试MIR-192-5P表达。进行过表达和敲低实验以确定MiR-192-5P对凋亡反应的影响。 H / R处理的H9C2细胞在miR-192-5p水平上表现出2.2倍。 MIR-192-5P的过度表达在H / R后显着增强了H9C2细胞中的细胞凋亡，其伴随着Bax / Bcl-2的比例的显着增加。相比之下，抗miR-192-5P抑制剂的递送显着降低了H / R诱导的细胞凋亡。 FABP3被鉴定为MIR-192-5P的功能靶标。 FABP3的恢复预防MIR-192-5P转染的H9C2细胞中的细胞凋亡，而在H / R暴露的H9C2细胞中的凋亡的下调增强凋亡。总之，MiR-192-5P通过靶向Fabp3介导H / R诱导的心肌细胞凋亡，并且代表了预防心肌I / R损伤的潜在靶标。

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