Overexpression of lncRNA Gm43050 alleviates apoptosis and inflammation response induced by sevoflurane treatment by regulating miR-640/ZFP91

Weiwei Xu; Yanling Zhao; Yanqiu Ai

Overexpression of lncRNA Gm43050 alleviates apoptosis and inflammation response induced by sevoflurane treatment by regulating miR-640/ZFP91

Am J Transl Res. 2020 Aug 15;12(8):4337-4346. eCollection 2020.

Authors

Weiwei Xu¹, Yanling Zhao¹, Yanqiu Ai¹

Affiliation

¹ Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University Zhengzhou, Henan, China.

PMID: 32913509
PMCID: PMC7476152

Abstract

Aims: The present study investigated the function and mechanism of lncRNA Gm43050 in sevoflurane-induced abnormal cognition.

Methods: Primary hippocampal neurons were used to establish the model of abnormal cognitive disorder. Overexpression and knockdown experiments were performed to analyze cell death rates, proliferation, apoptosis and the inflammatory response. The dual-luciferase reporter assay was used to analyze the potential binding targets of lncRNA Gm43050. Rescue experiments were used to assess the downstream targets of Gm43050.

Results: We found that lncRNA Gm43050 was in the cytoplasm. Overexpression of lncRNA Gm43050 had no impact on proliferation but significantly reduced the cell death rates and apoptosis. The inflammation markers IL-6, IL-1β, IL-8 and TNF-α were manifestly downregulated in the overexpression group. Opposite effects were detected in the lncRNA Gm43050 knockdown group. Bioinformatics analysis showed that miR-640 may be the potential target of Gm43050. Additionally, we found that ZFP91 was the downstream target of miR-640.

Conclusion: We provided comprehensive data of the function and mechanism of lncRNA Gm43050 in abnormal cognition. Our study showed that lncRNA Gm43050 exerted its important role via the regulation of miR-640 and ZFP91.

Keywords: Gm43050; Sevoflurane; ZFP91; miR-640.