Chemical Chaperone of Endoplasmic Reticulum Stress Inhibits Epithelial-Mesenchymal Transition Induced by TGF-beta 1 in Airway Epithelium via the c-Src Pathway
- Authors
- Lee, Heung-Man; Kang, Ju-Hyung; Shin, Jae-Min; Lee, Seoung-Ae; Park, Il-Ho
- Issue Date
- 2017
- Publisher
- HINDAWI LTD
- Citation
- MEDIATORS OF INFLAMMATION, v.2017
- Indexed
- SCIE
SCOPUS
- Journal Title
- MEDIATORS OF INFLAMMATION
- Volume
- 2017
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/132429
- DOI
- 10.1155/2017/8123281
- ISSN
- 0962-9351
- Abstract
- Epithelial-mesenchymal transition (EMT) is a biological process that allows epithelial cells to assume a mesenchymal cell phenotype. EMT is considered as a therapeutic target for several persistent inflammatory airway diseases related to tissue remodeling. Herein, we investigated the role of endoplasmic reticulum (ER) stress and c-Src in TGF-beta 1-induced EMT. A549 cells, primary nasal epithelial cells (PNECs), and inferior nasal turbinate organ cultures were exposed to 4-phenylbutylic acid (4PBA) or PP2 and then stimulated with TGF-beta 1. We found that E-cadherin, vimentin, fibronectin, and alpha-SMA expression was increased in nasal polyps compared to inferior turbinates. TGF-beta 1 increased the expression of EMT markers such as E-cadherin, fibronectin, vimentin, and alpha-SMA and ER stress markers (XBP-1s and GRP78), an effect that was blocked by PBA or PP2 treatment. 4-PBA and PP2 also blocked the effect of TGF-beta 1 on migration of A549 cells and suppressed TGF-beta 1-induced expression of EMT markers in PNECs and organ cultures of inferior turbinate. In conclusion, we demonstrated that 4PBA inhibits TGF-beta 1-induced EMT via the c-Src pathway in A549 cells, PNECs, and inferior turbinate organ cultures. These results suggest an important role for ER stress and a diverse role for TGF-beta 1 in upper airway chronic inflammatory disease such as CRS.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
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