PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a chronic, usually fatal lung disease of unknown etiology. The key effector cell in fibrogenesis is the myofibroblast. Therefore, the aim of our study was to examine the expression of α-SMA, PI3K, FAK and TGF-β1. in association with myofibroblast anti-apoptosis in IPF human patients.
METHODS: We examined by immunohistochemistry the expression of α-SMA, PI3K, FAK and TGF-β1 in lung specimens taken by biopsy in19 IPF patients and 12 control subjects. An independent tissue evaluation by two pathologists graded semiquantatively the degree of staining present.
RESULTS: The levels of the expression of α-SMA, PI3K, FAK and TGF-β1 protein were significantly higher in the IPF group than in the control group. There was positive correlation of the expression of α-SMA, PI3K, FAK and TGF-β1 protein. In addition, TGF-β1 have significantly positive correlation with PI3K and FAK in IPF patients.
CONCLUSIONS: TGF-β1 may protect myofibroblasts from anoikis by activation of the PI3K-AKT pathway. Moreover, in China, we firstly study the relationship between myofibroblast and PI3K, FAK,TGF-β1 expression in human IPF patients.
CLINICAL IMPLICATIONS: the development of more targeted approaches that interfere with fibrogenesis will help to combat this progressive, disabling and fatal disease.
DISCLOSURE: Xitao Ma: Other: provincial science fund
Juanjuan Ding: Other: provincial science fund
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