MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells.

It was previously demonstrated that microRNA-210 (miR-210) exhibited neuroprotective effects in a murine model of hypoxic-ischemic encephalopathy via inhibition of apoptosis. The aim of the present study was to further elucidate the effect of miR-210 on apoptosis in PC12 cells following transfection with miR-210 inhibitors and exposure to oxygen glucose deprivation (OGD). The expression levels of miR-210 were identified using reverse transcription-quantitative polymerase chain reaction analysis. Apoptosis was investigated using Annexin V-fluorescein isothiocyanate assays. Apoptosis-related protein expression levels were studied with western blot analysis. The results showed that the expression levels of miR-210 were upregulated in PC12 cells following a 4-h exposure to OGD, relative to those in normoxic control cells. miR-210 knockdown increased cell apoptosis by inducing caspase activity and regulating the balance between Bcl-2 and Bax levels. The present study demonstrated that miR-210 knockdown induced cell apoptosis using an ex vivo model of ischemic hypoxia (IH). Knockdown of miR-210 represents a potential novel therapeutic approach to combat neonatal IH.