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MicroRNA-218 Aggravates HO-induced Damage in PC12 Cells Via Spred2-mediated Autophagy

Overview
Journal Exp Ther Med
Specialty Pathology
Date 2021 Oct 18
PMID 34659498
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Abstract

The current study aimed to investigate the effects and underlying mechanism of miR-218 in HO-induced neuronal injury. The impacts of miR-218 knockdown on cell viability, apoptosis and autophagy-associated proteins were detected by Cell Counting Kit-8 assay, flow cytometry and western blotting in HO-injured PC12 cells, respectively. Reverse transcription-quantitative PCR (RT-qPCR) and western blotting was executed to explore the expression level of miR-218 and sprouty-related EVH1 domainprotein2 (spred2) in HO-stimulated cells. Besides, the regulatory association between miR-218 and spred2 was explored through bioinformatics and luciferase reporter assay. Following knockdown of miR-218 and spred2, the functions of miR-218 and spred2 in HO-injured cells were further studied. High expression level of miR-218 was observed in HO-disposed PC12 cells, while spred2 expression level was downregulated. Knockdown of miR-218 expression alleviated HO-induced PC12 cell injury by increasing cell proliferation, and decreasing apoptosis and autophagy. Furthermore, spred2 was identified as a direct target of miR-218 and was negatively regulated by miR-218. Moreover, suppression of spred2 abrogated the protective effects of miR-218 inhibition on HO-injured PC12 cells. Depletion of miR-218 protected PC12 cells against HO-induced cell injury via the upregulation of spred2, which provided a promising therapeutic strategy for spinal cord injury.

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