Aims: In previous studies, numerous differential microRNAs (miRNAs) in cerebral ischemic/reperfusion (I/R) injury were identified using the miRNA microarray analysis. However, the relationship between miRNA and cerebral I/R injury remains largely unknown. In this study, we investigated the function and explored the possible mechanism of miR-224-3p in cerebral I/R injury.
Methods: Oxygen glucose deprivation model in N2a cells were used to perform the cerebral I/R injury in vitro. Trypan blue staining, reactive oxygen species (ROS) production, and caspase-3 were measured to evaluate the function of miR-224-3p.
Results: Overexpression of miR-224-3p alleviated the apoptosis induced by oxygen glucose deprivation (OGD) and cleaved caspase-3 was significantly reduced. We further provided the possible mechanism that miR-224-3p may protect cells from cerebral I/R injury by targeting FAK family-interacting protein (FIP200). Further rescue experiment proved that overexpression of FIP200 partially blocked the effect of miR-224-3p.
Conclusions: We evaluated the function and mechanism of miR-224-3p in ischemic brain injury. miR-224-3p may serve as a potential target for new therapeutic intervention.
Keywords: FIP200; apoptosis; ischemic stroke; miR-224-3p.
© 2019 Wiley Periodicals, Inc.