MicroRNA-29c Correlates with Neuroprotection Induced by FNS by Targeting Both Birc2 and Bak1 in Rat Brain after Stroke

AimsStudies showed fastigial nucleus stimulation (FNS) reduced brain damage, but the mechanisms of neuroprotection induced by FNS were not entirely understood; MicroRNAs are noncoding RNA molecules that regulate gene expression in a posttranscriptional manner, but their functional consequence in response to ischemia-reperfusion (IR) remains unknown. We investigated the role of microRNA-29c in the neuroprotection induced by FNS in rat. MethodsThe IR rat models were conducted 1day after FNS. Besides, miR-29c antagomir (or agomir or control) was infused to the left intracerebroventricular 1day before IR models were conducted. We detected differential expression of Birc2 mRNA (also Bak1mRNA and miR-29c) level among different groups by RT-qPCR. The differential expression of Birc2 protein (also Bak1 protein) level among different groups was surveyed via Western blot. The neuroprotective effects were assessed by infarct volume, neurological deficit, and apoptosis. ResultsMiR-29c was decreased after FNS. Moreover, miR-29c directly bound to the predicted 3-UTR target sites of Birc2and Bak1 genes. Furthermore, over-expression of miR-29c effectively reduced Birc2 (also Bak1) mRNA and protein levels, increased infarct volume and apoptosis, and deteriorated neurological outcomes, whereas down-regulation played a neuroprotective role. ConclusionsMiR-29c correlates with the neuroprotection induced by FNS by negatively regulating Birc2 and Bak1.