Melatonin suppresses fibrotic responses induced by cigarette smoke via downregulation of TGF-β1

Cited 27 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorN R Shin-
dc.contributor.authorJi Won Park-
dc.contributor.authorIn Chul Lee-
dc.contributor.authorJ W Ko-
dc.contributor.authorS H Park-
dc.contributor.authorJ S Kim-
dc.contributor.authorJ C Kim-
dc.contributor.authorKyung Seop Ahn-
dc.contributor.authorI S Shin-
dc.date.accessioned2018-01-11T02:53:32Z-
dc.date.available2018-01-11T02:53:32Z-
dc.date.issued2017-
dc.identifier.issn1949-2553-
dc.identifier.uri10.18632/oncotarget.21680ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/17561-
dc.description.abstractCigarette smoke (CS) is the most important risk factor in the development of chronic obstructive pulmonary disease (COPD). Pulmonary fibrosis is an irreversible response and important feature of COPD. In this study, we investigated the effects of melatonin on fibrotic response in development of COPD using a CS and lipopolysaccharide (LPS) induced COPD model and cigarette smoke condensate (CSC)-stimulated NCI-H292 cells, a human mucoepidermoid cell line. Mice were exposed to CS for 1 h per day (8 cigarettes per day) from day 1 to day 7 and were treated intranasally with LPS on day 4. Melatonin (10 or 20 mg/kg) was injected intraperitoneally 1 h before CS exposure. Melatonin decreased the inflammatory cell counts in bronchoalveolar lavage fluid (BALF), with a reduction in transforming growth factor (TGF)-β1. Melatonin inhibited the expression of TGF-β1, collagen I and SMAD3 phosphorylation in lung tissue exposed to CS and LPS. In CSC-stimulated H292 cells, melatonin suppressed the elevated expression of fibrotic mediators induced by CSC treatment. Melatonin reduced the expression of TGF-β1, collagen I, SMAD3 and p38 phosphorylation in CSC-stimulated H292 cells. In addition, cotreatment with melatonin and TGF-β1 inhibitors significantly limited fibrotic mediators, with greater reductions in the expression of TGF-β1, collagen I, SMAD3 and p38 phosphorylation than those of H292 cells treated with TGF-β1 inhibitor alone. Taken together, melatonin effectively inhibited fibrotic responses induced by CS and LPS exposure, which was related to the downregulation of TGF-β1. Therefore, our results suggest that melatonin may suppress the pulmonary fibrotic response induced by CS-
dc.publisherImpact Journalsko
dc.titleMelatonin suppresses fibrotic responses induced by cigarette smoke via downregulation of TGF-β1-
dc.title.alternativeMelatonin suppresses fibrotic responses induced by cigarette smoke via downregulation of TGF-β1-
dc.typeArticle-
dc.citation.titleOncotarget-
dc.citation.number56-
dc.citation.endPage95703-
dc.citation.startPage95692-
dc.citation.volume8-
dc.contributor.affiliatedAuthorJi Won Park-
dc.contributor.affiliatedAuthorIn Chul Lee-
dc.contributor.affiliatedAuthorKyung Seop Ahn-
dc.contributor.alternativeName신나래-
dc.contributor.alternativeName박지원-
dc.contributor.alternativeName이인철-
dc.contributor.alternativeName고제원-
dc.contributor.alternativeName박성혁-
dc.contributor.alternativeName김중선-
dc.contributor.alternativeName김종춘-
dc.contributor.alternativeName안경섭-
dc.contributor.alternativeName신인식-
dc.identifier.bibliographicCitationOncotarget, vol. 8, no. 56, pp. 95692-95703-
dc.identifier.doi10.18632/oncotarget.21680-
dc.subject.keywordCigarette smoke-
dc.subject.keywordMAPK-
dc.subject.keywordMelatonin-
dc.subject.keywordPulmonary fibrosis-
dc.subject.keywordTGF-β1-
dc.subject.localcigarette smoke-
dc.subject.localCigarette smoke-
dc.subject.localMAPK-
dc.subject.localMAPKs-
dc.subject.localMelatonin-
dc.subject.localmelatonin-
dc.subject.localPulmonary fibrosis-
dc.subject.localpulmonary fibrosis-
dc.subject.localTGF-β1-
dc.subject.localTGFβ-1-
dc.description.journalClassN-
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.