miR-338–3p inhibits autophagy in a rat model of allergic rhinitis after PM2.5 exposure through AKT/mTOR signaling by targeting UBE2Q1

Exposure to fine particulate matter (PM2.5) increases the incidence of allergic rhinitis (AR). microRNA (miRNA) can regulate cell proliferation, invasion and apoptosis. However, the mechanism of miR-338–3p in mediating PM2.5-induced autophagy in AR animal models remains unknown. To explore the mechanism of miR-338–3p in PM2.5-induced autophagy in AR, the human nasal epithelium cells and AR model exposed to PM2.5 were deployed. The results showed that miR-338–3p was down-regulated in both nasal mucosa of PM2.5-exacerbated AR rat models and PM2.5-treated RPMI-2650 cells. Forced expression of miR-338–3p could inhibit autophagy in vitro. miR-338–3p specifically bound to UBE2Q1 3′-untranslated region (3′ UTR) and negatively regulated its expression. Overexpression of UBE2Q1 attenuated the inhibitory effects of miR-338–3p on PM2.5-induced autophagy of RPMI-2650 cells through AKT/mTOR pathway. Moreover, our in vivo study found that after administration of agomiR-338–3p in AR rats model, the expression of autophagy-related proteins decreased and nasal symptoms alleviated. In conclusion, this study revealed that miR-338–3p acts as an autophagy suppressor in PM2.5-exacerbated AR by directly targeting UBE2Q1 and affecting AKT/mTOR pathway. •PM2.5 can aggravate autophagy.•PM2.5 can inhibit the expression of miR-338–3p.•miR-338–3p agomiR can relieve nasal symptoms in AR model exposured to PM2.5•miR-338–3p/UBE2Q1/AKT/mTOR regulates PM2.5-induced autophagy.