MiRNA-190 exerts neuroprotective effects against ischemic stroke through Rho/Rho-kinase pathway

Ischemic stroke is an urgent public health concern and one of the major causes of deaths and disabilities over the world. MicroRNA (miRNA) has become a key mediator of cerebral ischemia-reperfusion (I/R) injuries. However, whether miR-190 is involved in cerebral I/R-induced neuronal damage remains unknown. This study was to investigate the role of miR-190 in the brain I/R injury. We divided the rats into sham, I/R, control, and miR-190-mim (miR-190 mimics) groups. Quantitative real-time polymerase chain reaction (qRT-PCR), Nissl staining, flow cytometry, and western blot were conducted to examine the expression of miR-190 and cell apoptosis in different groups. The results showed that the expression of miR-190 was greatly decreased in rats suffering with I/R. Overexpression of miR-190 significantly reduced the increased neurological scores, brain water contents, infarct volumes, and neuronal apoptosis in rats suffering with I/R. In addition, we found that the expression of RhoA and Rho kinase was greatly elevated in rats suffering with I/R. Bioinformatics analysis indicated that Rho was a target of miR-190. Moreover, overexpression of miR-190 significantly downregulated the increased mRNA and protein expression of Rho/Rho kinase and cell apoptosis, while inhibition of miR-190 further upregulated the increased mRNA and protein expression of Rho/Rho kinase and cell apoptosis in rats suffering with I/R. Furthermore, knockdown of Rho significantly downregulated the increased mRNA and protein expression of Rho/Rho kinase and cell apoptosis, while these effects were inhibited by miR-190 inhibitors in rats suffering with I/R. These results indicate that miR-190 confers protection against brain I/R damage by modulating Rho/Rho-kinase signaling.