A causal relationship between the neurotherapeutic effects of miR182/7a and decreased expression of PRDM5

Abstract

BackgroundSpinal cord injury (SCI) is terrible damage resulting in the deficiencies and necrosis of neurology and causes infinite inconvenience to sufferers. The therapy of SCI still meets a larger number of problems. Therefore, the underlying mechanism and novel therapy of acute SCI (ASCI) are urgent to explore. Materials and methodsThe SCI model was established in rats. The expression of miR-182/miR-7a and PRDM5 at mRNA level was detected by quantitative real-time PCR and the protein expression of PRDM5 and c-caspase 3 was assessed by western blotting assays. The apoptosis of spinal cord neurons (SCN) was assessed on flow cytometry. The transfection of cells was performed by Lipofectamine 2000 kit. The relationship between PRDM5 and miR-182/miR-7a was examined by Luciferase assay. ResultsThe expression of PRDM5 was up-regulated at either mRNA (2.212 folds) or protein level after SCI in rats, and knockdown of PRDM5 in SCN declined the c-caspase3 expression. In addition, the expression of miR-182 and miR-7a was decreased by 44.6% and 39.3% after SCI in rats. Moreover, the expression of miR-182 and miR-7a were negatively correlated with the level of PRDM5 expression, and the expression of PRDM5 was inhibited due to the increase of miR-182 and/or miR-7a expression. Moreover, both miR-182 and miR-7a could regulate PRDM5 to control SCN apoptosis. According to the BBB score increased 2 folds, the intrathecal injection of miR-182 and miR-7a improved the neurological function of rats. ConclusionInhibition of PRDM5 which was apparently negative correlation with miR-182 and miR-7a could suppress the neurons apoptosis to attenuate acute spinal cord injury in rats.