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dc.contributor.author김대기-
dc.date.accessioned2016-08-28T12:08:51Z-
dc.date.available2016-08-28T12:08:51Z-
dc.date.issued2011-
dc.identifier.issn0895-8378-
dc.identifier.otherOAK-7702-
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/221722-
dc.description.abstractOzone (O3), a commonly encountered environmental pollutant, has been shown to induce pulmonary fibrosis in different animal models; the underlying mechanism, however, remains elusive. To investigate the molecular mechanism underlying O3-induced pulmonary fibrosis, 6- to 8-week-old C57BL/6 male mice were exposed to a cyclic O3 exposure protocol consisting of 2 days of filtered air and 5 days of O3 exposure (0.5-ppm, 8-h/day) for 5 and 10 cycles with or without intraperitoneal injection of IN-1233, a specific inhibitor of the type 1 receptor of transforming growth factor beta (TGF-ββ), the most potent profibrogenic cytokine. The results showed that O3 exposure for 5 or 10 cycles increased the TGF-ββ protein level in the epithelial lining fluid (ELF), associated with an increase in the expression of plasminogen activator inhibitor 1 (PAI-1), a TGF-ββ-responsive gene that plays a critical role in the development of fibrosis under various pathological conditions. Cyclic O3 exposure also increased the deposition of collagens and alpha smooth muscle actin (αα-SMA) in airway walls. However, these fibrotic changes were not overt until after 10 cycles of O3 exposure. Importantly, blockage of the TGF-ββ signaling pathway with IN-1233 suppressed O3-induced Smad2/3 phosphorylation, PAI-1 expression, as well as collagens and αα-SMA deposition in the lung. Our data demonstrate for the first time that O3 exposure increases TGF-ββ expression and activates TGF-ββ signaling pathways, which mediates O3-induced lung fibrotic responses in vivo. © 2011 Informa Healthcare USA, Inc.-
dc.languageEnglish-
dc.titleIncreased transforming growth factor beta 1 expression mediates ozone-induced airway fibrosis in mice-
dc.typeArticle-
dc.relation.issue8-
dc.relation.volume23-
dc.relation.indexSCI-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage486-
dc.relation.lastpage494-
dc.relation.journaltitleInhalation Toxicology-
dc.identifier.doi10.3109/08958378.2011.584919-
dc.identifier.wosidWOS:000291807000005-
dc.identifier.scopusid2-s2.0-79959395509-
dc.author.googleKatre A.-
dc.author.googleBallinger C.-
dc.author.googleAkhter H.-
dc.author.googleFanucchi M.-
dc.author.googleKim D.-K.-
dc.author.googlePostlethwait E.-
dc.author.googleLiu R.-M.-
dc.contributor.scopusid김대기(35083694200)-
dc.date.modifydate20220303081001-
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약학대학 > 약학과 > Journal papers
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