MiR-92b-3p regulates oxygen and glucose deprivation-reperfusion-mediated apoptosis and inflammation by targeting TRAF3 in PC12 cells.

NEW FINDINGS What is the central question of this study? MiR-92b-3p was found to be reduced in a rat model of middle cerebral artery occlusion: what are the functions of miR-92b-3p in oxygen and glucose deprivation-reperfusion (OGD/R)? What is the main finding and its importance? MiR-92b-3p abated apoptosis, mitochondrial dysfunction and inflammation caused by OGD/R via targeting TRAF3, suggesting that miR-92b-3p may serve as a potential therapeutic target in ischaemic stroke treatment. ABSTRACT Stroke is the most common cause of human neurological disability. MiR-92b-3p has been shown to be decreased in a rat model of middle cerebral artery occlusion, but its effects in cerebral ischaemic insult are unknown. In this study, PC12 cells were exposed to oxygen and glucose deprivation-reperfusion (OGD/R) to establish cerebral ischaemic injury in vitro. Quantitative real time-PCR analysis demonstrated that OGD/R exposure led to down-regulation of miR-92b-3p and increased mRNA and protein levels of tumour necrosis factor receptor-associated factor 3 (TRAF3). Gain of miR-92b-3p expression facilitated cell survival; attenuated lactate dehydrogenase leakage, cell apoptosis, caspase 3 activity and cleaved-caspase 3 (c-caspase 3) expression; and decreased the Bax/Bcl-2 ratio. Furthermore, miR-92b-3p repressed mitochondrial membrane potential depolarization, reactive oxygen species production, cytochrome c protein expression, inflammatory cytokine production and the reduction of ATP content. MiR-92b-3p directly targeted the 3'-untranslated region of TRAF3 and decreased TRAF3 expression. Reinforced expression of TRAF3 partly abrogated the biological activity of miR-92b-3p during OGD/R. Hence, miR-92b-3p abated apoptosis, mitochondrial dysfunction and inflammatory responses induced by OGD/R by targeting TRAF3.