DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ha, Eun Hee | ko |
dc.contributor.author | Choi, Jun-Pyo | ko |
dc.contributor.author | Kwon, Hyouk-Soo | ko |
dc.contributor.author | Park, Hyeung Ju | ko |
dc.contributor.author | Lah, Sang Joon | ko |
dc.contributor.author | Moon, Keun-Ai | ko |
dc.contributor.author | Lee, Seung-Hyo | ko |
dc.contributor.author | Kim, Injune | ko |
dc.contributor.author | Cho, You Sook | ko |
dc.date.accessioned | 2019-08-20T06:20:05Z | - |
dc.date.available | 2019-08-20T06:20:05Z | - |
dc.date.created | 2019-08-19 | - |
dc.date.created | 2019-08-19 | - |
dc.date.issued | 2019-08 | - |
dc.identifier.citation | JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, v.144, no.2, pp.561 - + | - |
dc.identifier.issn | 0091-6749 | - |
dc.identifier.uri | http://hdl.handle.net/10203/264329 | - |
dc.description.abstract | Background: IL-33, levels of which are known to be increased in patients with eosinophilic asthma and which is suggested as a therapeutic target for it, activates endothelial cells in which Sry-related high-mobility-group box (Sox) 17, an endothelium-specific transcription factor, was upregulated. Objective: We investigated the relationship between Sox17 and IL-33 and the possible role of Sox17 in the pathogenesis of asthma using a mouse model of airway inflammation. Methods: We used ovalbumin (OVA) to induce airway inflammation in endothelium-specific Sox17 null mutant mice and used IL-33 neutralizing antibody to evaluate the interplay between IL-33 and Sox17. We evaluated airway inflammation and measured levels of various cytokines, chemokines, and adhesion molecules. We also carried out loss-or gain-of-function experiments for Sox17 in human endothelial cells. Results: Levels of IL-33 and Sox17 were significantly increased in the lungs of OVA-challenged mice. Anti-IL-33 neutralizing antibody treatment attenuated not only OVA-induced airway inflammation but also Sox17 expression in pulmonary endothelial cells. Importantly, endothelium-specific deletion of Sox17 resulted in significant alleviation of various clinical features of asthma, including airway inflammation, immune cell infiltration, cytokine/chemokine production, and airway hyperresponsiveness. Sox17 deletion also resulted in decreased densities of Ly6c(high) monocytes and inflammatory dendritic cells in the lungs. In IL-33-stimulated human endothelial cells, Sox17 showed positive correlation with CCL2 and intercellular adhesion molecule 1 levels. Lastly, Sox17 promoted monocyte adhesion to endothelial cells and upregulated the extracellular signal-regulated kinase-signal transducer and activator of transcription 3 pathway. Conclusion: Sox17 was regulated by IL-33, and its genetic ablation in endothelial cells resulted in alleviation of asthma-related pathophysiologic features. Sox17 might be a potential target for asthma management. | - |
dc.language | English | - |
dc.publisher | MOSBY-ELSEVIER | - |
dc.title | Endothelial Sox17 promotes allergic airway inflammation | - |
dc.type | Article | - |
dc.identifier.wosid | 000478789300023 | - |
dc.identifier.scopusid | 2-s2.0-85064597960 | - |
dc.type.rims | ART | - |
dc.citation.volume | 144 | - |
dc.citation.issue | 2 | - |
dc.citation.beginningpage | 561 | - |
dc.citation.endingpage | + | - |
dc.citation.publicationname | JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY | - |
dc.identifier.doi | 10.1016/j.jaci.2019.02.034 | - |
dc.contributor.localauthor | Lee, Seung-Hyo | - |
dc.contributor.localauthor | Kim, Injune | - |
dc.contributor.nonIdAuthor | Choi, Jun-Pyo | - |
dc.contributor.nonIdAuthor | Kwon, Hyouk-Soo | - |
dc.contributor.nonIdAuthor | Moon, Keun-Ai | - |
dc.contributor.nonIdAuthor | Cho, You Sook | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | Sox17 | - |
dc.subject.keywordAuthor | IL-33 | - |
dc.subject.keywordAuthor | asthma | - |
dc.subject.keywordAuthor | allergic airway inflammation | - |
dc.subject.keywordPlus | LUNG DENDRITIC CELLS | - |
dc.subject.keywordPlus | ASTHMA | - |
dc.subject.keywordPlus | IL-33 | - |
dc.subject.keywordPlus | ADHESION | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | DEFICIENCY | - |
dc.subject.keywordPlus | RESPONSES | - |
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