LncRNA GAS5 upregulates miR-214 through methylation to participate in cell apoptosis of sepsis

被引：45
作者：
Li, Min [1 ]
Zhang, Zhimin [2 ]
Liu, Boyi [1 ]
Chen, Li [1 ]
Wang, Menghe [3 ]
机构：
[1] Hubei Univ Med, Taihe Hosp, Dept Crit Care Med, Shiyan, Hubei, Peoples R China
[2] Hubei Univ Med, Affliated Dongfeng Hosp, Dept Crit Care Med, Shiyan, Hubei, Peoples R China
[3] Hubei Univ Med, Taihe Hosp, Dept Nursing, 32 Renmin South Rd, Shiyan 442000, Hubei, Peoples R China
来源：
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY | 2022年 / 128卷 / 05期
关键词：
GAS5; sepsis; cardiomyocytes; miR-124; methylation; apoptosis; SIGNALING PATHWAY; INJURY;
D O I：
10.1080/13813455.2020.1764051
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：1259 / 1264
页数：6
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