Effect of doxycycline on epithelial-mesenchymal transition via the p38/Smad pathway in respiratory epithelial cells
DC Field | Value | Language |
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dc.contributor.author | Shin, Jae-Min | - |
dc.contributor.author | Kang, Ju-Hyung | - |
dc.contributor.author | Lee, Seoung-Ae | - |
dc.contributor.author | Park, Il-Ho | - |
dc.contributor.author | Lee, Heung-Man | - |
dc.date.accessioned | 2021-09-03T08:40:43Z | - |
dc.date.available | 2021-09-03T08:40:43Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2017-03 | - |
dc.identifier.issn | 1945-8924 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/84211 | - |
dc.description.abstract | Purpose: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. Methods: A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and cellular morphologic changes. Western blot and immunofluorescence staining were used to determine the expression levels of E-cadherin, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cellular migration ability. Results: Doxycycline (0-10 mu g/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. Increased expression of mesenchymal markers, including vimentin, alpha-smooth muscle actin, and fibronectin in TGF beta 1 induced A549 cells were downregulated by doxycycline treatment. In contrast, E-cadherin expression was upregulated in TGF beta 1 induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited the ability of TGF beta 1 induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells. Conclusion: Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | OCEAN SIDE PUBLICATIONS INC | - |
dc.subject | EXTRACELLULAR-MATRIX PRODUCTION | - |
dc.subject | POLYP-DERIVED FIBROBLASTS | - |
dc.subject | TGF-BETA | - |
dc.subject | CHRONIC RHINOSINUSITIS | - |
dc.subject | AIRWAY EPITHELIUM | - |
dc.subject | FIBROSIS | - |
dc.subject | FAMILY | - |
dc.title | Effect of doxycycline on epithelial-mesenchymal transition via the p38/Smad pathway in respiratory epithelial cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Heung-Man | - |
dc.identifier.doi | 10.2500/ajra.2017.31.4410 | - |
dc.identifier.scopusid | 2-s2.0-85015762020 | - |
dc.identifier.wosid | 000397976100003 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF RHINOLOGY & ALLERGY, v.31, no.2, pp.71 - 77 | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF RHINOLOGY & ALLERGY | - |
dc.citation.title | AMERICAN JOURNAL OF RHINOLOGY & ALLERGY | - |
dc.citation.volume | 31 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 71 | - |
dc.citation.endPage | 77 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Otorhinolaryngology | - |
dc.relation.journalWebOfScienceCategory | Otorhinolaryngology | - |
dc.subject.keywordPlus | EXTRACELLULAR-MATRIX PRODUCTION | - |
dc.subject.keywordPlus | POLYP-DERIVED FIBROBLASTS | - |
dc.subject.keywordPlus | TGF-BETA | - |
dc.subject.keywordPlus | CHRONIC RHINOSINUSITIS | - |
dc.subject.keywordPlus | AIRWAY EPITHELIUM | - |
dc.subject.keywordPlus | FIBROSIS | - |
dc.subject.keywordPlus | FAMILY | - |
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