Abstrakt

Effect of microRNA125 in the proliferation and differentiation of neural stem cells damaged by ischemic stroke

Qiang Li, Bin Zhang, Kai Xie, Yanrong Chen, Shicong Zhou, Cuimei Sun

The repair of nervous system injury has been a hot and difficult topic. Our previous studies found that in ischemic stroke causes neural stem cell injury. MicroRNA125 expression level showed significant changes, suggesting microRNA125 may play a role in the regulating proliferation and differentiation of neural stem cells damaged by ischemic stroke. This study was to investigate the function and molecular mechanism of microRNA in the regulation of proliferation and differentiation of neural stem cells from patients with ischemic stroke. The rat model of ischemic stroke was established. Neural stem cells from ischemic stroke rats and control rats were collected. MicroRNA125 expression level was measured by RT-PCR. Rat neural stem cell RNSC-FMU1 was cultured and transfected with microRNA125. Flow cytometry and MTT assay were used to detect the apoptosis and proliferation of RNSC-FMU1 cells. The levels of microRNA125 in neural stem cells of ischemic stroke model were significantly higher than that of controls (P=0.017). Targeting microRNA125 by antisense siRNA reduced the growth of RNSC-FMU1 cells (P=0.0081) by induction of apoptosis (P=0.0082). Overexpression of microRNA125 promoted the growth of RNSC-FMU1 (P=0.019) and reduced the apoptosis (P=0.026). microRNA125 may be related to the repair of neural stem cells damaged by ischemic stroke. Decreasing the level of microRNA125 decreases the growth and proliferation of RNSC-FMU1 cells and induces RNSC-FMU1 cell apoptosis. Increasing the level of microRNA125 enhances the growth and proliferation of RNSC-FMU1 cells and reduces the apoptosis of RNSC-FMU1 cells.