Abstract

It has been reported that lncRNA GAS5 can inhibit LPS-induced inflammation, indicating its involvement in sepsis. We observed the downregulation of GAS5 in plasma of sepsis patients. In addition, expression levels of GAS5 were positively correlated with the expression levels of miR-214. In cardiomyocytes, overexpression of GAS5 upregulated the expression of miR-214, while its knockdown resulted in decreased expression levels of miR-124. Methylation-specific PCR (MSP) revealed that GAS5 negatively regulated the methylation of miR-124. Cell apoptosis showed that overexpression of GAS5 and miR-214 suppressed the apoptosis of cardiomyocytes induced by LPS. In addition, overexpression of miR-214 also reduced the enhancing effects of silencing of GAS5 on cell apoptosis. Therefore, GAS5 may upregulate miR-214 through methylation pathway to inhibit the apoptosis of cardiomyocytes in sepsis.

摘要

据报道，lncRNA GAS5可以抑制LPS诱导的炎症，表明其参与了败血症。我们观察到脓毒症患者血浆中 GAS5 的下调。此外，GAS5的表达水平与miR-214的表达水平呈正相关。在心肌细胞中，GAS5 的过表达上调了 miR-214 的表达，而其敲低导致 miR-124 的表达水平降低。甲基化特异性 PCR (MSP) 显示 GAS5 负调控 miR-124 的甲基化。细胞凋亡表明GAS5和miR-214的过表达抑制了LPS诱导的心肌细胞凋亡。此外，miR-214的过表达也降低了GAS5沉默对细胞凋亡的增强作用。所以，