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

Authors
 Woo-In Yang  ;  Dajeong Lee  ;  Da Lyung Lee  ;  Sung-Yu Hong  ;  Sang-Hak Lee  ;  Seok-Min Kang  ;  Dong-Hoon Choi  ;  Yangsoo Jang  ;  Se Hoon Kim  ;  Sungha Park 
Citation
 CIRCULATION JOURNAL, Vol.78(5) : 1197-1205, 2014 
Journal Title
 CIRCULATION JOURNAL 
ISSN
 1346-9843 
Issue Date
2014
MeSH
Animals ; Autoimmune Diseases/chemically induced ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Autoimmune Diseases/prevention & control* ; Gene Expression Regulation/immunology* ; Immunity, Innate* ; Male ; Myocarditis/chemically induced ; Myocarditis/immunology ; Myocarditis/pathology ; Myocarditis/prevention & control* ; Myocardium/immunology* ; Myocardium/pathology ; Rats ; Rats, Inbred Lew ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic/antagonists & inhibitors* ; Receptors, Immunologic/immunology ; Swine
Keywords
Immunology ; Myocarditis ; The Receptor for Advanced Glycation End Products
Abstract
Background: 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.
Files in This Item:
T201401091.pdf Download
DOI
10.1253/circj.CJ-13-1235
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) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
Yonsei Authors
Kang, Seok Min(강석민) ORCID logo https://orcid.org/0000-0001-9856-9227
Kim, Se Hoon(김세훈) ORCID logo https://orcid.org/0000-0001-7516-7372
Park, Sung Ha(박성하) ORCID logo https://orcid.org/0000-0001-5362-478X
Lee, Da Lyung(이다령)
Lee, Da Jeong(이다정)
Lee, Sang Hak(이상학) ORCID logo https://orcid.org/0000-0002-4535-3745
Jang, Yang Soo(장양수) ORCID logo https://orcid.org/0000-0002-2169-3112
Choi, Dong Hoon(최동훈) ORCID logo https://orcid.org/0000-0002-2009-9760
Hong, Sung Yu(홍성유)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/98588
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