The pathogenesis of CRS is not yet exact. microRNAs are widely involved in several physiological and pathological processes, of which miR-146a plays an essential role in innate immunity, inflammatory response, and other pathophysiological processes. MUCs are crucial components of secreted mucus, of which MUC5AC is the major MUC secreted in the normal airway. This study was performed to examine HNE-induced MUC5AC overexpression in CRS via miR-146a.
miR-146a, HNE, EGFR, and MUC5AC expressions in the sinonasal mucosa were determined using qRT-PCR. EGFR pEGFR and MUC5AC expressions were determined in primary cultures of HNECs. We examined the expression of miR-146a, MUC5AC, EGFR, and pEGFR by transfecting HNECs with miR-146a mimics and NC. Moreover, dual-luciferase reporter gene assays were used to validate EGFR as an hsa-miR-146a target gene.
The results of dual-luciferase reporter assays showed that the luciferase activities were markedly inhibited in the pGL3-EGFR-3′ UTR+miR-146a mimic group pGL3+ miR-146a mimic group, suggesting that EGFR is a target gene for miR-146a.
The study concluded that in HNE-induced CRS, miR-146a downregulates the expression of MUC5AC by inhibiting the activation of EGFR, and EGFR is a target gene of miR-146a.