Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation.
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. I...
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Public Library of Science (PLoS)
2017-01-01
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| author | Ting Wang Yuan Liu Jing-Feng Zou Zhen-Shun Cheng |
| author_facet | Ting Wang Yuan Liu Jing-Feng Zou Zhen-Shun Cheng |
| author_sort | Ting Wang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-d7c896e3c46447ac8edf43cfbb92aca1 |
| institution | DOAJ |
| issn | 1932-6203 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
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| series | PLoS ONE |
| spelling | doaj-art-d7c896e3c46447ac8edf43cfbb92aca12025-08-20T02:45:23ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01129e018397210.1371/journal.pone.0183972Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation.Ting WangYuan LiuJing-Feng ZouZhen-Shun ChengIdiopathic 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.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183972&type=printable |
| spellingShingle | Ting Wang Yuan Liu Jing-Feng Zou Zhen-Shun Cheng Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation. PLoS ONE |
| title | Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation. |
| title_full | Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation. |
| title_fullStr | Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation. |
| title_full_unstemmed | Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation. |
| title_short | Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation. |
| title_sort | interleukin 17 induces human alveolar epithelial to mesenchymal cell transition via the tgf β1 mediated smad2 3 and erk1 2 activation |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183972&type=printable |
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