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Archives of Physiology and Biochemistry
The Journal of Metabolic Diseases
Volume 128, 2022 - Issue 5
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Original Articles

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

, , , &
Pages 1259-1264 | Received 15 Feb 2020, Accepted 28 Apr 2020, Published online: 19 Jun 2020
 

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.

Acknowledgements

The authors thank the support from Taihe hospital.

Ethics approval

The present study was approved by the Ethics Committee of Taihe Hospital. The research has been carried out in accordance with the World Medical Association Declaration of Helsinki. All patients and healthy volunteers provided written informed consent prior to their inclusion within the study.

Disclosure statement

The authors declare that they have no competing interests.

Availability of data and materials

The analysed data sets generated during the study are available from the corresponding author on reasonable request.

Authors’ contributions

All authors contributed to data analysis, drafting or revising the article, gave final approval of the version to be published, and agree to be accountable for all aspects of the work.

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