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Cited 13 times in

Blocking the receptor for advanced glycation end product activation attenuates autoimmune myocarditis.

DC Field Value Language
dc.contributor.author강석민-
dc.contributor.author김세훈-
dc.contributor.author박성하-
dc.contributor.author이다령-
dc.contributor.author이다정-
dc.contributor.author이상학-
dc.contributor.author장양수-
dc.contributor.author최동훈-
dc.contributor.author홍성유-
dc.date.accessioned2015-01-06T16:41:47Z-
dc.date.available2015-01-06T16:41:47Z-
dc.date.issued2014-
dc.identifier.issn1346-9843-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/98588-
dc.description.abstractBackground: The Receptor for Advanced Glycation End Products (RAGE) is a pattern recognition receptor for endogenous ligands, and is associated with various inflammatory diseases. However, the role of RAGE activation in myocarditis has yet to be examined. The potential role of RAGE in the development of experimental autoimmune myocarditis (EAM) and the effect of RAGE blocking in attenuating the inflammation in the EAM was investigated. Methods and Results: EAM was evoked in Lewis rats by immunization with porcine cardiac myosin. Soluble RAGE (sRAGE) was injected to block RAGE activation. Echocardiogram, histological, and immunohistochemical examinations were conducted on days 21 and 42. In rats with EAM, RAGE expression in cardiac tissue was prominent on day 21. Rats administered sRAGE during the early antigen-priming phase showed marked attenuation in acute and chronic inflammation compared with untreated rats. RAGE expression was significantly reduced in rats treated in the early phase. However, sRAGE administration, after the initial antigen-priming phase, failed to ameliorate EAM development. Conclusions: RAGE expression was significantly increased in the heart during EAM. Blocking RAGE activation with sRAGE during the early antigen-priming phase reduced acute and chronic inflammation and improved cardiac function. In contrast, blocking RAGE after the early phase did not attenuate EAM development. These results imply that RAGE is involved in regulating innate immune responses during the early phase of myocarditis development.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1197~1205-
dc.relation.isPartOfCIRCULATION JOURNAL-
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.MESHAutoimmune Diseases/chemically induced-
dc.subject.MESHAutoimmune Diseases/immunology-
dc.subject.MESHAutoimmune Diseases/pathology-
dc.subject.MESHAutoimmune Diseases/prevention & control*-
dc.subject.MESHGene Expression Regulation/immunology*-
dc.subject.MESHImmunity, Innate*-
dc.subject.MESHMale-
dc.subject.MESHMyocarditis/chemically induced-
dc.subject.MESHMyocarditis/immunology-
dc.subject.MESHMyocarditis/pathology-
dc.subject.MESHMyocarditis/prevention & control*-
dc.subject.MESHMyocardium/immunology*-
dc.subject.MESHMyocardium/pathology-
dc.subject.MESHRats-
dc.subject.MESHRats, Inbred Lew-
dc.subject.MESHReceptor for Advanced Glycation End Products-
dc.subject.MESHReceptors, Immunologic/antagonists & inhibitors*-
dc.subject.MESHReceptors, Immunologic/immunology-
dc.subject.MESHSwine-
dc.titleBlocking the receptor for advanced glycation end product activation attenuates autoimmune myocarditis.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorWoo-In Yang-
dc.contributor.googleauthorDajeong Lee-
dc.contributor.googleauthorDa Lyung Lee-
dc.contributor.googleauthorSung-Yu Hong-
dc.contributor.googleauthorSang-Hak Lee-
dc.contributor.googleauthorSeok-Min Kang-
dc.contributor.googleauthorDong-Hoon Choi-
dc.contributor.googleauthorYangsoo Jang-
dc.contributor.googleauthorSe Hoon Kim-
dc.contributor.googleauthorSungha Park-
dc.identifier.doi10.1253/circj.CJ-13-1235-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00037-
dc.contributor.localIdA00610-
dc.contributor.localIdA01512-
dc.contributor.localIdA02707-
dc.contributor.localIdA02708-
dc.contributor.localIdA03448-
dc.contributor.localIdA04053-
dc.contributor.localIdA04400-
dc.contributor.localIdA02833-
dc.relation.journalcodeJ00534-
dc.identifier.eissn1347-4820-
dc.identifier.pmid24599045-
dc.subject.keywordImmunology-
dc.subject.keywordMyocarditis-
dc.subject.keywordThe Receptor for Advanced Glycation End Products-
dc.contributor.alternativeNameKang, Seok Min-
dc.contributor.alternativeNameKim, Se Hoon-
dc.contributor.alternativeNamePark, Sung Ha-
dc.contributor.alternativeNameLee, Da Lyung-
dc.contributor.alternativeNameLee, Da Jeong-
dc.contributor.alternativeNameLee, Sang Hak-
dc.contributor.alternativeNameJang, Yang Soo-
dc.contributor.alternativeNameChoi, Dong Hoon-
dc.contributor.alternativeNameHong, Sung Yu-
dc.contributor.affiliatedAuthorKang, Seok Min-
dc.contributor.affiliatedAuthorKim, Se Hoon-
dc.contributor.affiliatedAuthorPark, Sung Ha-
dc.contributor.affiliatedAuthorLee, Da Lyung-
dc.contributor.affiliatedAuthorLee, Da Jeong-
dc.contributor.affiliatedAuthorJang, Yang Soo-
dc.contributor.affiliatedAuthorChoi, Dong Hoon-
dc.contributor.affiliatedAuthorHong, Sung Yu-
dc.contributor.affiliatedAuthorLee, Snag Hak-
dc.citation.volume78-
dc.citation.number5-
dc.citation.startPage1197-
dc.citation.endPage1205-
dc.identifier.bibliographicCitationCIRCULATION JOURNAL, Vol.78(5) : 1197-1205, 2014-
dc.identifier.rimsid38132-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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