Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and usually progressive lung disease and the epithelial-mesenchymal transition (EMT) may play an important role in the pathogenesis of pulmonary fibrosis. IL-17 is a proinflammatory cytokine which promotes EMT profiles in lung inflammatory diseases. In this study, we investigated the effect of IL-17 on EMT in alveolar epithelial cell line A549 and the role of TGFβ1-Smad and ERK signaling pathways in the process. Morphological observation on the cells was performed under inverted microscope. The mRNA and protein expressions of E-cad and α-SMA were detected by quantitative RT-PCR and western blotting. The mRNA and protein expressions of TGF-β1 were analyzed via quantitative RT-PCR and ELISA. Expressions of Smad2/3, p-Smad2/3, ERK1/2, p-ERK1/2 and p-JNK were examined by western blotting. The results indicated that IL-17 can induce A549 cells to undergo morphological changes and phenotypic markers changes, such as down-regulated E-cad expression and up-regulated α-SMA expression. Additionally, IL-17 enhanced TGF-β1 expression and stimulated Smad2/3 and ERK1/2 phosphorylation in A549 cells. However, there were no significant differences in the expression of phosphorylated JNK in A549 cells with or without IL-17 treatment. SB431542 or U0126 treated cells showed inhibited morphological changes and phenotypic markers expression, such as up-regulated E-cad expression and down-regulated α-SMA expression. In summary, our results suggest that IL-17 can induce A549 alveolar epithelial cells to undergo EMT via the TGF-β1 mediated Smad2/3 and ERK1/2 activation.
Highlights
Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause [1]
To characterize the morphological changes stimulated by IL-17, we investigated the expression of phenotypic markers in A549 cells by Quantitative RT-PCR analysis
These results suggest that IL-17 initiated A549 cells to undergo epithelial-mesenchymal transition (EMT)
Summary
Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause [1]. Interleukin-17 and EMT pathogenesis of pulmonary fibrosis [3]. EMT is a process when epithelial cells gradually transform into mesenchymal-like cells losing their epithelial functionality and characteristics [4]. During this process, epithelial cells lose their characteristic cell-cell adhesion structures, change their polarity and cell-cell adhesion structures, and acquire a mesenchymal phenotype including a morphological transition from a cobblestone-like epithelial phenotype to a spindle-like mesenchymal phenotype, which is accompanied by the markers changes, such as the decreased expression of epithelial markers E-cadherin and the increased expression of mesenchymal markers α-SMA [5]
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