Journal
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Volume 128, Issue 5, Pages 1259-1264Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/13813455.2020.1764051
Keywords
GAS5; sepsis; cardiomyocytes; miR-124; methylation; apoptosis
Funding
- Taihe hospital
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Research has shown that GAS5 can upregulate the expression of miR-214 through methylation pathway, thereby inhibiting cardiomyocyte apoptosis in sepsis.
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.
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