Chemical Chaperone of Endoplasmic Reticulum Stress Inhibits Epithelial-Mesenchymal Transition Induced by TGF-beta 1 in Airway Epithelium via the c-Src Pathway
DC Field | Value | Language |
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dc.contributor.author | Lee, Heung-Man | - |
dc.contributor.author | Kang, Ju-Hyung | - |
dc.contributor.author | Shin, Jae-Min | - |
dc.contributor.author | Lee, Seoung-Ae | - |
dc.contributor.author | Park, Il-Ho | - |
dc.date.accessioned | 2021-12-21T16:41:20Z | - |
dc.date.available | 2021-12-21T16:41:20Z | - |
dc.date.created | 2021-08-30 | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 0962-9351 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/132429 | - |
dc.description.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. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | HINDAWI LTD | - |
dc.subject | UNFOLDED PROTEIN RESPONSE | - |
dc.subject | ER STRESS | - |
dc.subject | INFLAMMATION | - |
dc.subject | CELLS | - |
dc.subject | EMT | - |
dc.title | Chemical Chaperone of Endoplasmic Reticulum Stress Inhibits Epithelial-Mesenchymal Transition Induced by TGF-beta 1 in Airway Epithelium via the c-Src Pathway | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Heung-Man | - |
dc.contributor.affiliatedAuthor | Park, Il-Ho | - |
dc.identifier.doi | 10.1155/2017/8123281 | - |
dc.identifier.scopusid | 2-s2.0-85027148839 | - |
dc.identifier.wosid | 000406914300001 | - |
dc.identifier.bibliographicCitation | MEDIATORS OF INFLAMMATION, v.2017 | - |
dc.relation.isPartOf | MEDIATORS OF INFLAMMATION | - |
dc.citation.title | MEDIATORS OF INFLAMMATION | - |
dc.citation.volume | 2017 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | UNFOLDED PROTEIN RESPONSE | - |
dc.subject.keywordPlus | ER STRESS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | EMT | - |
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