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MicroRNA-20b-5p regulates propofol-preconditioning-induced inhibition of autophagy in hypoxia-and-reoxygenation-stimulated endothelial cells

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Abstract

Ischemia-reperfusion (IR) injury is a major cause of clinical emergencies during and after surgical procedures. Propofol protects the heart from cardiovascular IR injury by inhibiting autophagy. MicroRNAs (miRNAs) participate in anesthetic-regulated cardiovascular injury. MiR-20b-5p targets unc-51-like autophagy activating kinase 1 (ULK1). Its role in propofol-modulated cardiovascular IR injury remains unclear, however. In this study, we used an in vitro model of hypoxia-reoxygenation (HR)-induced injury to human umbilical vein endothelial cells (HUVECs) to determine the protective effect of miR-20b-5p in cells preconditioned with propofol. We found that miR-20b-5p was significantly higher and ULK1 was lower in propofol-preconditioned HUVECs with HR injury than in HUVECs with HR injury only. Additionally, miR-20b-5p overexpression increased cell viability and repressed autophagy and apoptosis more in propofol-preconditioned HUVECs with HR injury than in HUVECs with HR injury only. A luciferase reporter assay confirmed the target reaction between miR-20b-5p and ULK1. Overexpression of ULK1 restrained the protective effect of miR-20b-5p in propofol-preconditioned HUVECs with HR injury. In conclusion, our results indicate that propofol inhibits autophagic cell death via the miR-20b-5p-ULKI axis and that ULK1 may be a therapeutic target for cardiovascular IR injury.

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Acknowledgements

The authors would like to thank all members of department of anesthesiology in Shaanxi Provincial People’s Hospital for helpful discussions.

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Correspondence to Song Yulong.

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Communicated by Sorab Dalal

Corresponding editor: Sorab Dalal

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Zhen, W., Hui, D., Wenying, S. et al. MicroRNA-20b-5p regulates propofol-preconditioning-induced inhibition of autophagy in hypoxia-and-reoxygenation-stimulated endothelial cells. J Biosci 45, 35 (2020). https://doi.org/10.1007/s12038-020-9998-8

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  • DOI: https://doi.org/10.1007/s12038-020-9998-8

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