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EphA2 Receptor Signaling Mediates Inflammatory Responses in Lipopolysaccharide-Induced Lung Injury

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dc.contributor.author강영애-
dc.contributor.author김세규-
dc.contributor.author김영삼-
dc.contributor.author김은영-
dc.contributor.author박무석-
dc.contributor.author신미화-
dc.contributor.author장준-
dc.contributor.author정경수-
dc.contributor.author정지예-
dc.date.accessioned2018-03-26T17:10:02Z-
dc.date.available2018-03-26T17:10:02Z-
dc.date.issued2015-
dc.identifier.issn1738-3536-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/157273-
dc.description.abstractBACKGROUND: Eph receptors and ephrin ligands have several functions including angiogenesis, cell migration, axon guidance, fluid homeostasis, oncogenesis, inflammation and injury repair. The EphA2 receptor potentially mediates the regulation of vascular permeability and inflammation in response to lung injury. METHODS: Mice were divided into 3 experimental groups to study the role of EphA2 signaling in the lipopolysaccharide (LPS)-induced lung injury model i.e., IgG+phosphate-buffered saline (PBS) group (IgG instillation before PBS exposure), IgG+LPS group (IgG instillation before LPS exposure) and EphA2 monoclonal antibody (mAb)+LPS group (EphA2 mAb pretreatment before LPS exposure). RESULTS: EphA2 and ephrinA1 were upregulated in LPS-induced lung injury. The lung injury score of the EphA2 mAb+LPS group was lower than that of the IgG+LPS group (4.30±2.93 vs. 11.45±1.20, respectively; p=0.004). Cell counts (EphA2 mAb+LPS: 11.33×10(4)±8.84×10(4) vs. IgG+LPS: 208.0×10(4)±122.6×10(4); p=0.018) and total protein concentrations (EphA2 mAb+LPS: 0.52±0.41 mg/mL vs. IgG+LPS: 1.38±1.08 mg/mL; p=0.192) were decreased in EphA2 mAb+LPS group, as compared to the IgG+LPS group. In addition, EphA2 antagonism reduced the expression of phospho-p85, phosphoinositide 3-kinase 110γ, phospho-Akt, nuclear factor κB, and proinflammatory cytokines. CONCLUSION: This results of the study indicated a role for EphA2-ephrinA1 signaling in the pathogenesis of LPS-induced lung injury. Furthermore, EphA2 antagonism inhibits the phosphoinositide 3-kinase-Akt pathway and attenuates inflammation.-
dc.description.statementOfResponsibilityopen-
dc.languageKorean-
dc.publisher대한결핵 및 호흡기학회-
dc.relation.isPartOfTUBERCULOSIS AND RESPIRATORY DISEASES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleEphA2 Receptor Signaling Mediates Inflammatory Responses in Lipopolysaccharide-Induced Lung Injury-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Internal Medicine-
dc.contributor.googleauthorJi Young Hong-
dc.contributor.googleauthorMi Hwa Shin-
dc.contributor.googleauthorKyung Soo Chung-
dc.contributor.googleauthorEun Young Kim-
dc.contributor.googleauthorJi Ye Jung-
dc.contributor.googleauthorYoung Ae Kang-
dc.contributor.googleauthorYoung Sam Kim-
dc.contributor.googleauthorSe Kyu Kim-
dc.contributor.googleauthorJoon Chang-
dc.contributor.googleauthorMoo Suk Park-
dc.identifier.doi10.4046/trd.2015.78.3.218-
dc.contributor.localIdA00057-
dc.contributor.localIdA00602-
dc.contributor.localIdA00707-
dc.contributor.localIdA00811-
dc.contributor.localIdA01457-
dc.contributor.localIdA02102-
dc.contributor.localIdA03472-
dc.contributor.localIdA03570-
dc.contributor.localIdA03735-
dc.relation.journalcodeJ02761-
dc.identifier.eissn2005-6184-
dc.identifier.pmid26175775-
dc.subject.keywordEphA2 Protein-
dc.subject.keywordLipopolysaccharides-
dc.subject.keywordLung Injury-
dc.contributor.alternativeNameKang, Young Ae-
dc.contributor.alternativeNameKim, Se Kyu-
dc.contributor.alternativeNameKim, Young Sam-
dc.contributor.alternativeNameKim, Eun Young-
dc.contributor.alternativeNamePark, Moo Suk-
dc.contributor.alternativeNameShin, Mi Hwa-
dc.contributor.alternativeNameChang, Joon-
dc.contributor.alternativeNameJung, Kyung Soo-
dc.contributor.alternativeNameJung, Ji Ye-
dc.contributor.affiliatedAuthorKang, Young Ae-
dc.contributor.affiliatedAuthorKim, Se Kyu-
dc.contributor.affiliatedAuthorKim, Young Sam-
dc.contributor.affiliatedAuthorKim, Eun Young-
dc.contributor.affiliatedAuthorPark, Moo Suk-
dc.contributor.affiliatedAuthorShin, Mi Hwa-
dc.contributor.affiliatedAuthorChang, Joon-
dc.contributor.affiliatedAuthorJung, Kyung Soo-
dc.contributor.affiliatedAuthorJung, Ji Ye-
dc.citation.volume78-
dc.citation.number3-
dc.citation.startPage218-
dc.citation.endPage226-
dc.identifier.bibliographicCitationTUBERCULOSIS AND RESPIRATORY DISEASES, Vol.78(3) : 218-226, 2015-
dc.identifier.rimsid42313-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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