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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 H 2 O 2  was added to induce oxidative stress. TUNEL assay and qRT-PCR showed H 2 O 2  induced apoptosis and up-regulated miR-100 in a dose-dependent manner in RGC-5 cells. Conversely, lentiviral-mediated miR-100 down-regulation protected H 2 O 2  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 H 2 O 2  induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation.

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