MiR-181a inhibits human trabecular meshwork cell apoptosis induced by H₂O₂ through the suppression of NF-κB and JNK pathways

The trabecular meshwork (TM) plays a critical role in the outflow of aqueous humor. In this study, we aimed to investigate the effect of miR-181a on H2O2-induced apoptosis in TM cells. Human primary explant-derived TM cells were cultured in fibroblast medium and then treated with different concentrations of H2O2 for 2 h. We used a series of methods to carry out the research, such as MTT assay, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), apoptosis assay, and western blot methodology. The apoptosis assay and qRT-PCR showed that H2O2-induced apoptosis and cell viability were suppressed in a dose-dependent manner in TM cells. After the TM cells were treated with H2O2, miR-181a expression was significantly lower. The overexpression of miR-181a enhanced TM cells' viability, while the knockdown of miR-181a inhibited viability of cells. The overexpression of miR-181a suppressed TM cell apoptosis, while the knockdown of miR-181a induced apoptosis. H2O2 activated the nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) pathways and induced cell apoptosis, while the overexpression of miR-181a suppressed both pathways and decreased the rate of apoptosis. In conclusion, this study indicated that miR-181a could improve the survival rate of TM cells after H2O2 treatment by blocking the NF-κB and JNK signaling pathways. These findings might provide novel therapeutic opportunities in the treatment of glaucoma.