摘要
Abstract
OBJECTIVE To detect the effects of miR-107 on the proliferation, apoptosis and inflammatory factors of human nasal mucosal epithelial cells(HNMECs) induced by Lipopolysaccharides(LPS), and to elucidate the potential molecular mechanism. METHODS The expression changes of miR-107 and HMGBl(High mobility group box 1) in 1 mg/L LPS induced HNMECs before and after LPS induction were detected by using quantitative realtime PCR. LPS induced-HNMECs were transfected with miR-107 agomir and agomir control, and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide(MTT) assay, flow cytometry and enzyme-linked immunosorbent assay(ELISA) were performed to detect cell proliferation, apoptosis and inflammatory factors. Dual luciferase reporter assay and Western blots were applied to verify whether HMGB1 was a target gene of miR-107. RESULTS The expression of miR-107 in HNMECs after LPS induction was significantly lower than that before induction(t =9.35, P ＜0.05), while the expression of HMGB1 in HNMECs after LPS induction was significantly higher than that before induction(t =13.07, P＜0.05). Compared with transfected agomir control, transfection of miR-107 agomir in HNMECs significantly inhibited cell proliferation (F =17.12, P ＜0.05) and decreased inflammatory factor TNF-α(t =6.11, P ＜0.05). IL-1β(t =6.90, P ＜0.05) and IL-6(t =8.18, P ＜0.05) expression levels, and increased apoptosis rate(t =7.49, P ＜0.05). HMGB1 was a target gene of miR-107, and transfection of miR-107 agomir in HNMECs after LPS induction could significantly reduce the expression of HMGB1 protein (t =28.56, P ＜0.05). CONCLUSION miR-107 is upregulated in HNMECs after LPS induction, while HMGB1 is down-regulated. Overexpression of miR-107 significantly inhibits the proliferation of HNMECs and the expression of inflammatory factors after LPS induction, and promotes apoptosis. HMGB1 is a target gene of miR-107, suggesting that miR-107 may play a regulatory role by regulating HMGB1.关键词
miR-107/HMGBl/HNMECs/靶基因/炎症因子微小RNAKey words
miR-107/HMGBl/HNMECs/target gene/inflammatory factors microRNA
