Downregulation of microRNA-100 protects apoptosis and promotes neuronal growth in retinal ganglion cells.

BACKGROUND

Retinal ganglion cells (RGCs) are preferentially lost in glaucoma or optic neuritis. In the present study, we investigated the protective effect of mircoRNA 100 (miR-100) against oxidative stress induced apoptosis in RGC-5 cells.

RESULTS

Rat RGC-5 cells were cultured in plates and H2O2 was added to induce oxidative stress. TUNEL assay and qRT-PCR showed H2O2 induced apoptosis and up-regulated miR-100 in a dose-dependent manner in RGC-5 cells. Conversely, lentiviral-mediated miR-100 down-regulation protected H2O2 induced apoptosis, promoted neurite growth and activated AKT/ERK and TrkB pathways through phosphorylation. Luciferase assay confirmed that IGF1R was directly regulated by miR-100 in RGC-5 cells, and siRNA-mediated IGF1R knockdown activated AKT protein through phosphorylation, down-regulated miR-100, therefore exerted a protective effect on RGC-5 apoptosis.

CONCLUSION

Down-regulating miR-100 is an effective method to protect H2O2 induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation.