{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T22:09:11Z","timestamp":1790460551202,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003621","name":"Ministry of Science, ICT and Future Planning","doi-asserted-by":"publisher","award":["R1513641"],"award-info":[{"award-number":["R1513641"]}],"id":[{"id":"10.13039\/501100003621","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","award":["R1513641"],"award-info":[{"award-number":["R1513641"]}],"id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2017]]},"abstract":"<jats:p>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-<jats:italic>\u03b2<\/jats:italic>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-<jats:italic>\u03b2<\/jats:italic>1. We found that E-cadherin, vimentin, fibronectin, and <jats:italic>\u03b1<\/jats:italic>-SMA expression was increased in nasal polyps compared to inferior turbinates. TGF-<jats:italic>\u03b2<\/jats:italic>1 increased the expression of EMT markers such as E-cadherin, fibronectin, vimentin, and <jats:italic>\u03b1<\/jats:italic>-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-<jats:italic>\u03b2<\/jats:italic>1 on migration of A549 cells and suppressed TGF-<jats:italic>\u03b2<\/jats:italic>1-induced expression of EMT markers in PNECs and organ cultures of inferior turbinate. In conclusion, we demonstrated that 4PBA inhibits TGF-<jats:italic>\u03b2<\/jats:italic>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-<jats:italic>\u03b2<\/jats:italic>1 in upper airway chronic inflammatory disease such as CRS.<\/jats:p>","DOI":"10.1155\/2017\/8123281","type":"journal-article","created":{"date-parts":[[2017,7,19]],"date-time":"2017-07-19T17:02:32Z","timestamp":1500483752000},"page":"1-9","source":"Crossref","is-referenced-by-count":19,"title":["Chemical Chaperone of Endoplasmic Reticulum Stress Inhibits Epithelial-Mesenchymal Transition Induced by TGF-<i>\u03b2<\/i>1 in Airway Epithelium via the c-Src Pathway"],"prefix":"10.1155","volume":"2017","author":[{"given":"Heung-Man","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul, Republic of Korea"},{"name":"Department of Biomedical Sciences, Korea University Graduate School, Seoul, Republic of Korea"},{"name":"Medical Devices Clinical Trial Center, Guro Hospital, Korea University, Seoul, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ju-Hyung","family":"Kang","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Korea University Graduate School, Seoul, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jae-Min","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seoung-Ae","family":"Lee","sequence":"additional","affiliation":[{"name":"Medical Devices Clinical Trial Center, Guro Hospital, Korea University, Seoul, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7011-6071","authenticated-orcid":true,"given":"Il-Ho","family":"Park","sequence":"additional","affiliation":[{"name":"Department of 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