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首页> 外文期刊>Cellular Physiology and Biochemistry >MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells
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MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

机译：MicroRNA-145通过靶向H9c2细胞中的Rac1加重缺氧性损伤。

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>Background/Aims: Myocardial infarction (MI) is a leading cause of morbidity and mortality. Here, we sought to explore the potential role and underlying mechanism of miR-145 in MI. Methods: H9c2 cells were cultured under persistent hypoxia to simulate MI. The hypoxia-induced injury was assessed on the basis of cell viability, migration, invasion and apoptosis. The expression of miR-145 was evaluated by qRT-PCR and the influence of aberrantly expressed miR-145 on H9c2 cells under hypoxia was also estimated. Utilizing bioinformatics methods, the target genes of miR-145 were verified by luciferase reporter assay. Then, effects of abnormally expressed target gene on miR-145 silenced H9c2 cells were assessed. Finally, the phosphorylation levels of key kinases in the phosphatidylinositol-3-kinase (PI3K)/AKT and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathways were detected by Western blot analysis. Results: Hypoxia remarkably lowered viability, migration and invasion but promoted cell apoptosis. Meantime, the miR-145 level was up-regulated in H9c2 cells under hypoxia. Following experiments suggested that hypoxia-induced injury was exacerbated by miR-145 overexpression while was alleviated by miR-145 silence. Rac1 was predicted and further validated to be a target gene of miR-145. The influence of miR-145 silencing on H9c2 cells under hypoxia could be reversed by down-regulation of Rac1. Additionally, the phosphorylation levels of PI3K, AKT, MAPK and ERK were all elevated in miR-145 silenced cells and these alterations were reversed by down-regulation of Rac1. Conclusion: miR-145 silencing could protect H9c2 cells against hypoxia-induced injury by targeting Rac1, in which PI3K/AKT and MAPK/ERK pathways might be involved.
机译：> 背景/目的： 心肌梗塞（MI）是发病率和死亡率的主要原因。在这里，我们试图探索miR-145在MI中的潜在作用和潜在机制。 方法： 在持续缺氧条件下培养H9c2细胞以模拟MI。根据细胞活力，迁移，侵袭和凋亡来评估低氧诱导的损伤。通过qRT-PCR评估miR-145的表达，并评估缺氧条件下miR-145异常表达对H9c2细胞的影响。利用生物信息学方法，通过荧光素酶报告基因分析验证了miR-145的靶基因。然后，评估异常表达的靶基因对miR-145沉默的H9c2细胞的作用。最后，通过蛋白质印迹分析检测了磷脂酰肌醇-3-激酶（PI3K）/ AKT和丝裂原激活的蛋白激酶（MAPK）/细胞外信号调节激酶（ERK）途径中关键激酶的磷酸化水平。 结果： 缺氧显着降低了细胞的活力，迁移和侵袭能力，但促进了细胞凋亡。同时，在缺氧条件下，H9c2细胞中的miR-145水平上调。以下实验表明，miR-145过表达会加剧缺氧性损伤，而miR-145沉默则会减轻缺氧引起的损伤。 Rac1被预测并进一步证实是miR-145的靶基因。缺氧下miR-145沉默对H9c2细胞的影响可以通过下调Rac1来逆转。此外，在miR-145沉默的细胞中，PI3K，AKT，MAPK和ERK的磷酸化水平均升高，而这些改变可通过下调Rac1来逆转。 结论： miR-145沉默可以通过靶向Rac1来保护H9c2细胞免受低氧诱导的损伤，其中PI3K / AKT和MAPK / ERK途径可能参与其中。

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