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Inhibition of EphA2/EphrinA1 signal attenuates lipopolysaccharide-induced lung injury

DC Field Value Language
dc.contributor.author강영애-
dc.contributor.author장준-
dc.contributor.author정경수-
dc.contributor.author정지예-
dc.contributor.author김세규-
dc.contributor.author김영삼-
dc.contributor.author김은영-
dc.contributor.author박무석-
dc.date.accessioned2017-10-26T07:36:00Z-
dc.date.available2017-10-26T07:36:00Z-
dc.date.issued2016-
dc.identifier.issn0143-5221-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/152254-
dc.description.abstractEph-Ephrin signalling mediates various cellular processes, including vasculogenesis, angiogenesis, cell migration, axon guidance, fluid homoeostasis and repair after injury. Although previous studies have demonstrated that stimulation of the EphA receptor induces increased vascular permeability and inflammatory response in lung injury, the detailed mechanisms of EphA2 signalling are unknown. In the present study, we evaluated the role of EphA2 signalling in mice with lipopolysaccharide (LPS)-induced lung injury. Acute LPS exposure significantly up-regulated EphA2 and EphrinA1 expression. Compared with LPS+IgG mice (IgG instillation after LPS exposure), LPS+EphA2 mAb mice [EphA2 monoclonal antibody (mAb) instillation posttreatment after LPS exposure] had attenuated lung injury and reduced cell counts and protein concentration of bronchoalveolar lavage fluid (BALF). EphA2 mAb posttreatment down-regulated the expression of phosphoinositide 3-kinases (PI3K) 110γ, phospho-Akt, phospho-NF-κB p65, phospho-Src and phospho-S6K in lung lysates. In addition, inhibiting the EphA2 receptor augmented the expression of E-cadherin, which is involved in cell-cell adhesion. Our study identified EphA2 receptor as an unrecognized modulator of several signalling pathways-including PI3K-Akt-NF-kB, Src-NF-κB, E-cadherin and mTOR-in LPS-induced lung injury. These results suggest that EphA2 receptor inhibitors may function as novel therapeutic agents for LPS-induced lung injury.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherPortland Press-
dc.relation.isPartOfCLINICAL SCIENCE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHBronchoalveolar Lavage Fluid/chemistry-
dc.subject.MESHEphrin-A1/metabolism*-
dc.subject.MESHHumans-
dc.subject.MESHLipopolysaccharides/adverse effects*-
dc.subject.MESHLung/metabolism-
dc.subject.MESHLung Injury/genetics-
dc.subject.MESHLung Injury/metabolism*-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHReceptor, EphA2/antagonists & inhibitors-
dc.subject.MESHReceptor, EphA2/genetics-
dc.subject.MESHReceptor, EphA2/metabolism*-
dc.subject.MESHSignal Transduction-
dc.titleInhibition of EphA2/EphrinA1 signal attenuates lipopolysaccharide-induced lung injury-
dc.typeArticle-
dc.publisher.locationEngland-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Internal Medicine-
dc.contributor.googleauthorJi Young Hong-
dc.contributor.googleauthorMi Hwa Shin-
dc.contributor.googleauthorIvor S. Douglas-
dc.contributor.googleauthorKyung Soo Chung-
dc.contributor.googleauthorEun Young Kim-
dc.contributor.googleauthorJi Ye Jung-
dc.contributor.googleauthorYoung Ae Kang-
dc.contributor.googleauthorSe Kyu Kim-
dc.contributor.googleauthorJoon Chang-
dc.contributor.googleauthorYoung Sam Kim-
dc.contributor.googleauthorMoo Suk Park-
dc.identifier.doi10.1042/CS20160360-
dc.contributor.localIdA03472-
dc.contributor.localIdA03570-
dc.contributor.localIdA03735-
dc.contributor.localIdA00602-
dc.contributor.localIdA00707-
dc.contributor.localIdA00811-
dc.contributor.localIdA01457-
dc.contributor.localIdA00057-
dc.relation.journalcodeJ00613-
dc.identifier.eissn1470-8736-
dc.identifier.pmid27549114-
dc.identifier.urlhttp://www.clinsci.org/content/130/21/1993-
dc.subject.keywordEphA2-
dc.subject.keywordEphrinA1-
dc.subject.keywordacute lung injury-
dc.subject.keywordlipopolysaccharide-
dc.contributor.alternativeNameKang, Young Ae-
dc.contributor.alternativeNameChang, Joon-
dc.contributor.alternativeNameJung, Kyung Soo-
dc.contributor.alternativeNameJung, Ji Ye-
dc.contributor.alternativeNameKim, Se Kyu-
dc.contributor.alternativeNameKim, Young Sam-
dc.contributor.alternativeNameKim, Eun Young-
dc.contributor.alternativeNamePark, Moo Suk-
dc.contributor.affiliatedAuthorChang, Joon-
dc.contributor.affiliatedAuthorJung, Kyung Soo-
dc.contributor.affiliatedAuthorJung, Ji Ye-
dc.contributor.affiliatedAuthorKim, Se Kyu-
dc.contributor.affiliatedAuthorKim, Young Sam-
dc.contributor.affiliatedAuthorKim, Eun Young-
dc.contributor.affiliatedAuthorPark, Moo Suk-
dc.contributor.affiliatedAuthorKang, Young Ae-
dc.citation.volume130-
dc.citation.number21-
dc.citation.startPage1993-
dc.citation.endPage2003-
dc.identifier.bibliographicCitationCLINICAL SCIENCE, Vol.130(21) : 1993-2003, 2016-
dc.date.modified2017-10-24-
dc.identifier.rimsid47991-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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