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2017 ; 12
(9
): e0183972
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Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition
via the TGF-?1 mediated Smad2/3 and ERK1/2 activation
#MMPMID28873461
Wang T
; Liu Y
; Zou JF
; Cheng ZS
PLoS One
2017[]; 12
(9
): e0183972
PMID28873461
show ga
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 TGF?1-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 ?-SMA were detected by quantitative
RT-PCR and western blotting. The mRNA and protein expressions of TGF-?1 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 ?-SMA expression. Additionally, IL-17 enhanced TGF-?1 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 ?-SMA expression. In summary, our results
suggest that IL-17 can induce A549 alveolar epithelial cells to undergo EMT via
the TGF-?1 mediated Smad2/3 and ERK1/2 activation.