Journal
EXPERIMENTAL LUNG RESEARCH
Volume 36, Issue 1, Pages 12-24Publisher
TAYLOR & FRANCIS INC
DOI: 10.3109/01902140903042589
Keywords
alveolar epithelial cell; cell contractility; epithelial mesenchymal transition; pulmonary fibrosis; TGF-beta 1; TNF-alpha
Categories
Funding
- Ministry of Education, Science, Sports, Culture and Technology of Japan
- Ministry of Health, Labour and Welfare, Japan
- Research on Allergic Disease and Immunology
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Recently, epithelial-mesenchymal transition (EMT) has been reported to contribute to tissue fibrosis through enhanced transforming growth factor (TGF)-beta 1 signaling. Tumor necrosis factor (TNF)-alpha has also been implicated in tissue fibrosis. Therefore, the authors investigated whether TNF-alpha affected TGF-beta 1-induced EMT. Cultured alveolar epithelial cells (A549 cells) were stimulated with TGF-beta 1 (5 ng/mL), with/without TNF-alpha (10 ng/mL). TGF-beta 1 induced EMT of A549 cells, with loss of E-cadherin and acquisition of vimentin. Combination of TNF-alpha with TGF-beta 1 enhanced EMT, causing morphological changes, while quantitative polymerase chain reaction (PCR) showed suppression of E-cadherin mRNA and expression of vimentin mRNA. In addition, the gel contraction method revealed that cells that had undergone EMT acquired cell contractility, which is a feature of mesenchymal cells. Stimulation with TGF-beta 1 induced cell contraction, as did TNF-alpha. Moreover, costimulation with TGF-beta 1 and TNF-alpha enhanced the cell contraction. Although IFN-gamma suppressed spontaneous cell contraction, it did not suppress cell contraction, which was induced by TGF-beta 1. In conclusion, TNF-alpha enhances not only EMT but also cell contraction induced by TGF-beta 1. EMT might contribute to tissue fibrosis through induction of cell contraction.
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