Neutralization of interleukin-1beta in the acute phase of myocardial infarction promotes the progression of left ventricular remodeling.
J Am Coll Cardiol
; 38(5): 1546-53, 2001 Nov 01.
Article
en En
| MEDLINE
| ID: mdl-11691538
ABSTRACT
OBJECTIVES:
We sought to examine the role of the pro-inflammatory cytokine, interleukin-1-beta (IL-1beta), in the process of left ventricular (LV) remodeling in the early phase after myocardial infarction (MI).BACKGROUND:
Studies have shown that pro-inflammatory cytokines are closely related to the progression of LV remodeling after MI.METHODS:
Mice underwent coronary artery ligation, and the time course of LV remodeling was followed up to 20 weeks. The gene expression level of IL-1beta was examined. In a second set of experiments, the mice underwent coronary artery ligation followed by treatment with anti-IL-1beta antibody (100 microg, intravenously), versus control immunoglobulin G (100 microg, intravenously) immediately after the operation.RESULTS:
Rapid hypertrophy of noninfarcted myocardium was observed by four weeks, and interstitial fibrosis progressed steadily up to 20 weeks. Anti-IL-1beta treatment increased the occurrence of ventricular rupture and suppressed collagen accumulation in the infarct-related area. At four and eight weeks after the operation, total heart weight and LV end-diastolic dimension were significantly greater in the anti-IL-1beta-treated mice than in the other groups. In the infarct-related area, collagen accumulation was suppressed, whereas in the noninfarcted area, pro-collagen gene expression levels, particularly type III, were decreased in the anti-IL-1beta-treated mice.CONCLUSIONS:
Anti-IL-1beta treatment suppressed pro-collagen gene expression and delayed wound healing mechanisms-properties that are likely to lead to progression of LV remodeling. In the acute phase of MI, IL-1beta appears to play a protective role.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Interleucina-1
/
Remodelación Ventricular
/
Modelos Animales de Enfermedad
/
Anticuerpos Monoclonales
/
Infarto del Miocardio
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Am Coll Cardiol
Año:
2001
Tipo del documento:
Article
País de afiliación:
Japón