title: [Silica induced α-SMA expression in HBE cell line by targeting the PI3K/Akt pathway].
abstract: OBJECTIVE
  To explore the role of the phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) pathway in silica-induced α-SMA (α 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 24 h 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 were found for TGFβ expressions. 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.
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Ai-ping
authors.initials: AP
authors.lastname: Li
authors.forename: Zhi-guo
authors.initials: ZG
authors.lastname: Hou
authors.forename: Jing-jing
authors.initials: JJ
authors.lastname: Fan
authors.forename: Xiao-ming
authors.initials: XM
authors.lastname: Ji
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.forename: Chun-hui
authors.initials: CH
authors.lastname: Ni
mesh_terms: D000199:Actins / Q000378:metabolism*; D002460:Cell Line; D002867:Chromones / Q000494:pharmacology; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D009025:Morpholines / Q000494:pharmacology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction; D012822:Silicon Dioxide / Q000633:toxicity*; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D000199:Actins; D002867:Chromones; D009025:Morpholines; D016212:Transforming Growth Factor beta; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D012822:Silicon Dioxide; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt