Potential roles for lncRNA Mirg/Foxp1 in an ARHL model created using C57BL/6J mice hearing research

Age-related hearing loss (ARHL) is involved in the hair cell apoptosis, but the underlying mechanism of hair cell apoptosis remains unclear. Here, we explored expression profiles of lncRNAs and mRNAs in an ARHL mouse model by using RNA sequencing and found that the cell apoptosis signaling pathway was activated in the cochlea tissues of old mice compared with those of young mice. We further found that lncRNA Mirg was most correlated with the cell apoptosis signaling pathway by the coexpression analysis. LncRNA Mirg was increased in the cochlea tissues of old mice compared with those of young mice, and its overexpression promoted hair cell apoptosis. H2O2-induced oxidative stress increased hair cell apoptosis by upregulating lncRNA Mirg. Furthermore, the expression of lncRNA Mirg and Foxp1 had the maximal correlation coefficient in the cochlea tissues of old mice, and lncRNA Mirg promoted hair cell apoptosis by increasing Foxp1 expression. In conclusion, we identified that oxidative stress-induced lncRNA Mirg promoted hair cell apoptosis via increasing Foxp1 expression, and these suggest that the lncRNA Mirg/Foxp1 signal may be a potential therapeutic target for ARHL. Expression profiles of lncRNAs and mRNAs in the basal parts of cochlear cochleae of age-related hearing loss