MicroRNAs (miRNAs) have been reported as key gene regulators, and they control many fundamental biological processes. Previously, we demonstrated that miR-214 had a protective effect against myocardial apoptosis and myocardial fibrosis. In this study, we sought to investigate the expression of miR-214 in L6 skeletal myoblast (SKM), the regulatory effect of miR-214 on hydrogen peroxide (H₂O₂) induced cell apoptosis and the underlying mechanisms of the antiapoptotic effect. MiR-214 expression was up-regulated by H₂O₂ in a dose and time-dependent manner in L6 SKMs. To investigate the regulatory effects of miR-214 on L6 SKM, both gain-of-function and loss-of-function approaches were applied. The results showed that miR-214 improved cell survival and inhibited cell apoptosis, and blockage of miR-214 abrogated the protective effect on cell survival and resistance to apoptosis. Phosphatase and tensin homolog (PTEN) was negatively regulated by miR-214, and PTEN inhibitor obviously reversed the effect of miR-214 blockage on enhancing cell apoptosis. In addition, miR-214 up-regulated antiapoptotic protein Bcl-2, down-regulated proapoptotic protein Bax, prevented release of cytochrome c and inhibited caspase-3 activation. In summary, H₂O₂-induced injury increases miR-214 expression in L6 SKM, and miR-214 contributes to the protection of L6 SKM against apoptosis via lowering PTEN and subsequently inhibiting the mitochondrial-mediated caspase-dependent apoptotic signaling pathway.

MicroRNA（miRNA）已被报道为关键的基因调节剂，它们控制着许多基本的生物学过程。以前，我们证明了miR-214对心肌细胞凋亡和心肌纤维化具有保护作用。在这项研究中，我们试图研究miR-214在L6骨骼肌成肌细胞（SKM）中的表达，miR-214对过氧化氢（H ₂ O ₂）诱导的细胞凋亡的调节作用以及抗凋亡作用的潜在机制。H ₂ O ₂上调了MiR-214的表达在L6 SKM中呈剂量依赖性和时间依赖性。为了研究miR-214对L6 SKM的调节作用，应用了功能获得和功能丧失方法。结果表明，miR-214改善了细胞存活并抑制了细胞凋亡，而miR-214的阻断则取消了对细胞存活和抗凋亡的保护作用。磷酸酶和张力蛋白同源物（PTEN）被miR-214负调节，并且PTEN抑制剂明显逆转了miR-214阻断增强细胞凋亡的作用。此外，miR-214上调抗凋亡蛋白Bcl-2，下调促凋亡蛋白Bax阻止了细胞色素c的释放并抑制了caspase-3的活化。总之，H ₂ O ₂诱导的损伤增加了L6 SKM中miR-214的表达，而miR-214通过降低PTEN并随后抑制线粒体介导的caspase依赖性凋亡信号通路，有助于保护L6 SKM免受凋亡。