Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice.
J Clin Invest
; 105(8): 1049-56, 2000 Apr.
Article
en En
| MEDLINE
| ID: mdl-10772649
ABSTRACT
Macrophage scavenger receptors have been implicated as key players in the pathogenesis of atherosclerosis. To assess the role of the class B scavenger receptor CD36 in atherogenesis, we crossed a CD36-null strain with the atherogenic apo E-null strain and quantified lesion development. There was a 76.5% decrease in aortic tree lesion area (Western diet) and a 45% decrease in aortic sinus lesion area (normal chow) in the CD36-apo E double-null mice when compared with controls, despite alterations in lipoprotein profiles that often correlate with increased atherogenicity. Macrophages derived from CD36-apo E double-null mice bound and internalized more than 60% less copper-oxidized LDL and LDL modified by monocyte-generated reactive nitrogen species. A similar inhibition of in vitro lipid accumulation and foam cell formation after exposure to these ligands was seen. These results support a major role for CD36 in atherosclerotic lesion development in vivo and suggest that blockade of CD36 can be protective even in more extreme proatherogenic circumstances.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Arteriosclerosis
/
Receptores Inmunológicos
/
Antígenos CD36
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Revista:
J Clin Invest
Año:
2000
Tipo del documento:
Article
País de afiliación:
Estados Unidos