Blocking the receptor for advanced glycation end product activation attenuates autoimmune myocarditis
| Autor: | Yangsoo Jang, Sungha Park, Se Hoon Kim, Donghoon Choi, Sang Hak Lee, Seok Min Kang, Sung Yu Hong, Dajeong Lee, Da Lyung Lee, Woo-In Yang |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Cardiac function curve
Male medicine.medical_specialty Myocarditis endocrine system diseases Swine Receptor for Advanced Glycation End Products Inflammation RAGE (receptor) Autoimmune Diseases chemistry.chemical_compound Glycation Internal medicine medicine Animals cardiovascular diseases Receptors Immunologic Receptor business.industry Myocardium Pattern recognition receptor nutritional and metabolic diseases General Medicine medicine.disease Immunity Innate Rats Endocrinology chemistry Gene Expression Regulation Rats Inbred Lew cardiovascular system Advanced glycation end-product medicine.symptom Cardiology and Cardiovascular Medicine business human activities |
| Zdroj: | Circulation journal : official journal of the Japanese Circulation Society. 78(5) |
| ISSN: | 1347-4820 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|