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OBJECTIVE: To determine the role of extracellular signal regulated kinase (ERK) signaling pathway in SiO₂ induced epithelial-mesenchymal transition (EMT) in human bronchial epithelial cells (HBEC) in vitro. METHODS: HBEC were treated with SiO₂ (0-300 μg/mL) for 72 h or pretreated with U0126 (0-30 μmol/L) for 1 h and then treated with 200 μg/mL SiO₂ for 72 h. Western blot was used to detect the protein expression of E-cadherin and α-smooth muscle actin (α-SMA). The activity of ERK was examined by mitogen-activated protein kinase (MAPK) activity assay kit in HBEC exposing to SiO₂ (200 μg/mL) for 0-8 h. RESULTS: The expression of E-cadherin decreased gradually in SiO₂ -stimulated HBEC, and the effect was most significant at 300 μg/mL (P<0.01). The expression of α-SMA increased and the effect was most evident at 200 μg/mL (P<0.01). With SiO₂ treatment, the activity of ERK was upregulated significantly. The phosphorylation of ERK increased at 30 min and decreased after 1 h. U0126 significantly inhibited SiO₂ -induced expression changes in E-cadherin and α-SMA. At 30 μmol/L, the effect was most evident(P<0.01). CONCLUSION ERK signaling pathway mediated EMT induced by SiO₂ in HBEC.
Actins ; metabolism ; Bronchi ; cytology ; Cadherins ; metabolism ; Cell Transdifferentiation ; drug effects ; Cells, Cultured ; Epithelial Cells ; cytology ; physiology ; Epithelial-Mesenchymal Transition ; Humans ; MAP Kinase Signaling System ; physiology ; Mitogen-Activated Protein Kinases ; metabolism ; Silicon Dioxide ; pharmacology