Apolipoprotein A1 Inhibits TGF-beta 1-Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells
DC Field | Value | Language |
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dc.contributor.author | Baek, Ae Rin | - |
dc.contributor.author | Lee, Ji Min | - |
dc.contributor.author | Seo, Hyun Jung | - |
dc.contributor.author | Park, Jong Sook | - |
dc.contributor.author | Lee, June Hyuk | - |
dc.contributor.author | Park, Sung Woo | - |
dc.contributor.author | Jang, An Soo | - |
dc.contributor.author | Kim, Do Jin | - |
dc.contributor.author | Koh, Eun Suk | - |
dc.contributor.author | Uh, Soo Taek | - |
dc.contributor.author | Kim, Yong Hoon | - |
dc.contributor.author | Park, Choon Sik | - |
dc.date.accessioned | 2021-09-10T05:24:22Z | - |
dc.date.available | 2021-09-10T05:24:22Z | - |
dc.date.issued | 2016-07 | - |
dc.identifier.issn | 1738-3536 | - |
dc.identifier.issn | 2005-6184 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/18647 | - |
dc.description.abstract | Background: Idiopathic pulmonary fibrosis (IPP) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor beta 1 (TGF-beta 1)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we deteimine whether ApoA1 modulates TGF-beta 1-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGE-beta 1 with or without ApoAl. Morphological changes and expression of EN/If-related markers, including E-cadherin, N-cadherin, and alpha-smooth muscle actin were evaluated. Expressions of Salad and non-Smad mediators and TGF-beta 1 receptor type I (T beta RI) and type 2 (T beta RII) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-beta 1-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-beta 1-induced change of the EMT phenotype. ApoA1 inhibited the TGF-beta 1-induced increase in the phosphorvlation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-beta 1-induced increase in T beta RI and T beta RII expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGFT-beta 1-induced EMT in experimental lung fibrosis. | - |
dc.format.extent | 10 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | 대한결핵및호흡기학회 | - |
dc.title | Apolipoprotein A1 Inhibits TGF-beta 1-Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells | - |
dc.type | Article | - |
dc.publisher.location | 대한민국 | - |
dc.identifier.doi | 10.4046/trd.2016.79.3.143 | - |
dc.identifier.scopusid | 2-s2.0-84978413848 | - |
dc.identifier.wosid | 000406830100005 | - |
dc.identifier.bibliographicCitation | Tuberculosis and Respiratory Diseases, v.79, no.3, pp 143 - 152 | - |
dc.citation.title | Tuberculosis and Respiratory Diseases | - |
dc.citation.volume | 79 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 143 | - |
dc.citation.endPage | 152 | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART002127670 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Respiratory System | - |
dc.relation.journalWebOfScienceCategory | Respiratory System | - |
dc.subject.keywordPlus | IDIOPATHIC PULMONARY-FIBROSIS | - |
dc.subject.keywordPlus | MOLECULAR TARGETS | - |
dc.subject.keywordPlus | BETA | - |
dc.subject.keywordPlus | FIBROBLASTS | - |
dc.subject.keywordPlus | PATHWAYS | - |
dc.subject.keywordPlus | FOCUS | - |
dc.subject.keywordPlus | EMT | - |
dc.subject.keywordAuthor | Apolipoprotein A-1 | - |
dc.subject.keywordAuthor | Transforming Growth Factor Betal | - |
dc.subject.keywordAuthor | Epithelial-Mesenchymal Transition | - |
dc.subject.keywordAuthor | Pulmonary Fibrosis | - |
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