DOWN-REGULATION OF MIR-100 INHIBITS THE APOPTOSIS OF GLAUCOMA RETINAL NEURONS BY INHIBITING THE EXPRESSION OF TARGET GENE ICF1R TO ACTIVATE THE TRKB/AKT/ERK SIGNALING PATHWAY

Objective: To investigate the down-regulation of miR-100 by inhibiting the expression of target gene ICF1R to activate the TrkB/ AKT/ERK signaling pathway to inhibit the apoptosis of glaucoma retinal neurons. Methods: Retinal neuron cells were cultured, 400 mu m hydrogen peroxide was applied to the retinal neuron cells for 24 h to construct an oxidative damage model, cells were transfected with miR-100 inhibitor and ICF1R inhibitor, and a corresponding negative control group was established. The real-time quantitative PCR method was used to detect the expression of miR-10 in retinal neurons of each group; MTT method was used to detect the effect of inhibiting apoptosis of miR-100 and ICF1R cells; Western blot analysis was used to measure the effect of inhibition of miR-100 on the TrkB/AKT/ERK signaling pathway. Results: The miR-100 mRNA expression in the miR-100 inhibitor group was significantly lower than that in the negative control group, and the difference was statistically significant (P<0.05). The apoptosis rate of retinal neurons in the miR-100 inhibitor group was significantly lower than that in the negative control group, and the difference was statistically significant (P<0.01). The phosphorylation levels of TrkB, AKT, and ERK1/2 in the miR-100 inhibitor group were significantly higher than those in the negative control group, and the difference was statistically significant (P<0.05). The expression of miR-100 in retinal neurons of ICF1R inhibitor group was significantly lower than that of negative control group, the difference was statistically significant (P<0.05). The apoptosis rate of retinal neurons in the ICF1R inhibitor group was significantly lower than that in the negative control group, the difference was statistically significant (P<0.05). Conclusion: Down-regulation of miR-100 expression can always inhibit the apoptosis of glaucoma retinal neurons. The mechanism may be that it inhibits the expression of ICF1R and activates the TrkB/AKT/ERK signaling pathway to protect cells.