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All-trans retinoic acid attenuates bleomycin-induced pulmonary fibrosis via downregulating EphA2-EphrinA1 signaling

DC Field Value Language
dc.contributor.author강영애-
dc.contributor.author김영삼-
dc.contributor.author김은영-
dc.contributor.author박무석-
dc.contributor.author송주한-
dc.contributor.author임아영-
dc.contributor.author장준-
dc.contributor.author정경수-
dc.contributor.author정지예-
dc.contributor.author신미화-
dc.date.accessioned2018-07-20T07:52:28Z-
dc.date.available2018-07-20T07:52:28Z-
dc.date.issued2017-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/160618-
dc.description.abstractThe role of all-trans retinoic acid (ATRA) in pulmonary fibrosis is relatively unknown, although this metabolite modulates cell differentiation, proliferation, and development. We aimed to evaluate the role of ATRA in bleomycin-induced pulmonary fibrosis, and whether the mechanism involves EphA2-EphrinA1 and PI3K-Akt signaling. We evaluated three groups of mice: a control group (intraperitoneal DMSO injection 3 times weekly after PBS instillation), bleomycin group (intraperitoneal DMSO injection 3 times weekly after bleomycin instillation), and bleomycin + ATRA group (intraperitoneal ATRA injection 3 times weekly after bleomycin instillation). The cell counts and protein concentration in the bronchoalveolar lavage fluid (BALF), changes in histopathology, Ashcroft score, hydroxyproline assay, expression of several signal pathway proteins including EphA2-EphrinA1, and PI3K-Akt, and cytokine levels were compared among the groups. We found that bleomycin significantly increased the protein concentration in the BALF, Ashcroft score in lung tissue, and hydroxyproline contents in lung lysates. Furthermore, bleomycin upregulated EphA2, EphrinA1, PI3K 110γ, Akt, IL-6 and TNF-α. However, administration of ATRA attenuated the upregulation of EphA2-EphrinA1 and PI3K-Akt after bleomycin instillation, and decreased pulmonary fibrosis. In addition, ATRA suppressed IL-6 and TNF-α production induced by bleomycin-induced injury. Collectively, these data suggest that ATRA attenuates bleomycin-induced pulmonary fibrosis by regulating EphA2-EphrinA1 and PI3K-Akt signaling.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCytokines/metabolism*-
dc.subject.MESHDown-Regulation/drug effects-
dc.subject.MESHEphrin-A1/metabolism*-
dc.subject.MESHLung/drug effects-
dc.subject.MESHLung/metabolism-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHPulmonary Fibrosis/chemically induced-
dc.subject.MESHPulmonary Fibrosis/metabolism*-
dc.subject.MESHPulmonary Fibrosis/prevention & control*-
dc.subject.MESHReceptor, EphA2/metabolism*-
dc.subject.MESHSignal Transduction/drug effects-
dc.subject.MESHTretinoin/administration & dosage*-
dc.titleAll-trans retinoic acid attenuates bleomycin-induced pulmonary fibrosis via downregulating EphA2-EphrinA1 signaling-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Internal Medicine-
dc.contributor.googleauthorAh Young Leem-
dc.contributor.googleauthorMi Hwa Shin-
dc.contributor.googleauthorIvor S. Douglas-
dc.contributor.googleauthorJoo Han Song-
dc.contributor.googleauthorKyung Soo Chung-
dc.contributor.googleauthorEun Young Kim-
dc.contributor.googleauthorJi Ye Jung-
dc.contributor.googleauthorYoung Ae Kang-
dc.contributor.googleauthorJoon Chang-
dc.contributor.googleauthorYoung Sam Kim-
dc.contributor.googleauthorMoo Suk Park-
dc.identifier.doi10.1016/j.bbrc.2017.07.122-
dc.contributor.localIdA00057-
dc.contributor.localIdA00707-
dc.contributor.localIdA00811-
dc.contributor.localIdA01457-
dc.contributor.localIdA02062-
dc.contributor.localIdA03382-
dc.contributor.localIdA03472-
dc.contributor.localIdA03570-
dc.contributor.localIdA03735-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid28743499-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0006291X17314808-
dc.subject.keywordAll-trans retinoic acid-
dc.subject.keywordBleomycin-
dc.subject.keywordEphA2-
dc.subject.keywordEphrinA1-
dc.subject.keywordPulmonary fibrosis-
dc.contributor.alternativeNameKang, Young Ae-
dc.contributor.alternativeNameKim, Young Sam-
dc.contributor.alternativeNameKim, Eun Young-
dc.contributor.alternativeNamePark, Moo Suk-
dc.contributor.alternativeNameSong, Joo Han-
dc.contributor.alternativeNameLeem, Ah Young-
dc.contributor.alternativeNameChang, Joon-
dc.contributor.alternativeNameJung, Kyung Soo-
dc.contributor.alternativeNameJung, Ji Ye-
dc.contributor.affiliatedAuthorKang, Young Ae-
dc.contributor.affiliatedAuthorKim, Young Sam-
dc.contributor.affiliatedAuthorKim, Eun Young-
dc.contributor.affiliatedAuthorPark, Moo Suk-
dc.contributor.affiliatedAuthorSong, Joo Han-
dc.contributor.affiliatedAuthorLeem, Ah Young-
dc.contributor.affiliatedAuthorChang, Joon-
dc.contributor.affiliatedAuthorJung, Kyung Soo-
dc.contributor.affiliatedAuthorJung, Ji Ye-
dc.citation.volume491-
dc.citation.number3-
dc.citation.startPage721-
dc.citation.endPage726-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.491(3) : 721-726, 2017-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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