The effects of silencing circANKRD11 on RSV-induced bronchial epithelial cell damage by targeting miR-218-5p

ZHAO Meng; LI Yanhong

doi:10.13431/j.cnki.immunol.j.20230124

Abstract：This study was designed to explore the effect of silencing circANKRD11 on bronchial epithelial cell damage induced by respiratory syncytial virus(RSV)and its possible mechanism.Human bronchial epithelial cells(HBECs)induced by RSV were cultured for 24 h in medium with RSV of 0.000 1 MOI after corresponding transfection to construct cell damage model.qRT-PCR method was used to detect the expression of circANKRD11,miR-218-5p,TNFR1 and BRD4;CCK-8 method and flow cytometry were used to detect cell proliferation and apoptosis;ELISA method was used to detect the levels of IL-6 and IL-1β.Furthermore,the dual luciferase reporter experiment was used to detect the targeting relationship between circANKRD11 and miR-218-5p;Western blot method was used to detect the expression of Bax,Bcl-2,TNFR1,and BRD4 protein.Data showed that the expression of circANKRD11,TNFR1 and BRD4 in RSV-induced HBECs was increased(P<0.05),while the expression of miR-218-5p was decreased(P<0.05).After transfection of si-circANKRD11 or miR-218-5p mimic,reductions in cell proliferation inhibition rate,IL-6 level,IL-1β level and apoptosis rate were observed in RSV-induced HBECs(P<0.05).circANKRD11 could act as a molecular sponge to targeting bind to miR-218-5p.The introduction of miR-218-5p inhibitor in cells was able to abolish the effects of si-circANKRD11 transfection on the proliferation,apoptosis and inflammation of RSV-induced HBECs.Taken together,silencing of circANKRD11 could promote cell proliferation and inhibit cell apoptosis and inflammation by decreasing TNFR1 and BRD4 level via elevating miR-218-5p level,thereby reducing RSV-induced bronchial epithelial cell damage.