• Jin Li and Lishan Ma.
• Department of Internal Neurology, Wuwei People's Hospital, Wuwei, Gansu, China.
• World Neurosurg. 2020 Apr 1; 136: e149-e157.

BackgroundmiR-142-3p has been reported to be involved in several diseases, including cardiac hypertrophy and several tumors, but whether it exerts neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury remains unclear.MethodsIn this study, the neuronal cell line SH-SY5Y was exposed to 6 hours of oxygen and glucose deprivation followed by 24 hours of reoxygenation (OGD/R) to mimic I/R injury in vitro. MiR-142-3p mimics were used to up-regulate the expression of miR-142-3p in SH-SY5Y cells before OGD/R induction. The changes in cell viability, apoptosis, and inflammation were assessed by CCK-8, lactate dehydrogenase (LDH), flow cytometry, and enzyme-linked immunosorbent assays.ResultsWe found that miR-142-3p expression was decreased after OGD/R induction. miR-142-3p overexpression significantly protected SH-SY5Y cells against OGD/R-induced cell injury, as reflected by improved cell viability and reduced LDH leakage, proinflammatory cytokines, and apoptosis. Mechanistically, bioinformatics analysis and a dual luciferase reporter assay confirmed F-box protein 3 (FBXO3) as the target gene of miR-142-3p. Direct siRNA-mediated silencing of FBXO3 exerted a protective role against OGD/R-induced injury. Moreover, FBXO3 overexpression significantly reversed the protective effects of miR-142-3p against OGD/R-induced cell injury.ConclusionsmiR-142-3p-mediated down-regulation of FBXO3 may be a potential agent for protection against cerebral I/R injury.Copyright © 2019 Elsevier Inc. All rights reserved.

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