长链非编码 RNA GAS5 通过甲基化上调 miR-214 参与脓毒症细胞凋亡。
LncRNA GAS5 upregulates miR-214 through methylation to participate in cell apoptosis of sepsis.
机构信息
Department of Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
Department of Critical Care Medicine, Affliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
出版信息
Arch Physiol Biochem. 2022 Oct;128(5):1259-1264. doi: 10.1080/13813455.2020.1764051. Epub 2020 Jun 19.
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.
已有报道称，lncRNA GAS5 可抑制 LPS 诱导的炎症，表明其参与了败血症的发生。我们观察到败血症患者血浆中 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，而其敲低则导致 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。细胞凋亡实验表明，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 的过表达也降低了沉默 GAS5 对细胞凋亡的增强作用。因此，GAS5 可能通过甲基化途径上调 miR-214 来抑制败血症中心肌细胞的凋亡。
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