[Silica induced α-SMA expression in HBE cell line by targeting the PI3K/Akt pathway].

Objective To explore the role of the phosphotidylinositol 3 kinase/protein kinase B (PI3K/Akt) pathway in silica-induced α-SMA (c smooth muscle actin) expression in HEB (human bronchial epithelial)cell.Methods The cultured HBE cells were divided into 5 groups:control,silica,PI3K inhibitor (Ly294002),both PI3K inhibitor (Ly294002) and silica at the same time and the inhibitor 24h ahead of silica.The final concentrations of PI3K inhibitor and silica were 10 μmol/L and 100 μg/ml,respectively.Western blots were used to detect protein expressions of Akt,p-Akt,TGF-β and α-SMA.The location and expression of α-SMA were measured by immunofluorescence assay.Results HBE cell line exposed to silica can induce Akt phosphorylation,in which expressions of p-Akt were up regulated 1 times at 48 and the highest at 72 h.The expressions of TGFβ increased remarkably at 12 h and the peak at 48 h after silica exposure,while the expressions of α-SMA increased at 24 h and the highest at 72 h.However,the PI3K inhibitor (Ly294002) significantly down regulated α-SMA expression.When the cell line exposed to the PI3K inhibitor ahead of silica 24 h,the expressions of p-Akt and α-SMA were more remarkably down regulated which were decreased 1.5 times and 7.6 times respectively compare to silica exposure group.But no significant changes werc found for TGFβexpressions.The immunofluorescence assay showed that silica can induce α-SMA expression,which located in cytoplasma,and PI3K inhibitor can decrease the expression.Conclusions Silica induced α-SMA expression in HBE cell line is by targeting the PI3K/Akt pathway and PI3K inhibitor can repress α-SMA expression. Key words: 1-Phosphatidylinositol 3-kinase;  Signaling system;  Silicon olioxide;  Actins;  PI3K/Akt pathway