Purpose Oxidative stress plays a very important role in the progress of Age related macular degeneration（AMD）. Nerve growth factor is critical for the survival and maintenance of sympathetic and sensory neurons. In this study, we investigated whether NGF play a critical role in AMD prevention and treatment and the possible involved signaling pathway.
Methods Cultured RPE cells were pretreated with H2O2 or not followed by treatment with NGF and then subjected to cell migration assay by phagokinetci track mobility assay. Cell viability was assessed using the tetrazolium salt 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide dye (MTT) assay. PI3K/AKT/mTOR pathway was analyzed by SDS-PAGE/Western blot and confocal.
Results Using cultured human retina pigment epithelial cells, we demonstrate that NGF could induce cell viability against H2O2-induced apoptosis. And NGF could also induce the migration of RPE which may play a role in retina regernation. We observed that NGF upregulated P-S6 in a time- and dose dependent. While, NGF also protects agasinst a H2O2-induced decrease expresstion of P-S6. The pharmacologic inhibitor of PI3K or mTOR inhibitors NGF-induced P-S6 activation and attenuates the nuroprotect effect of NGF against H2O2-induced cell damage.
Concusion Collectively, we conclude that NGF attenuates H2O2-induced cell damage including cell viability and migration via activating mtor pathway. Understanding the cellular signaling pathways may reveal potential therapeutic effect of NGF in AMD.