Targeted disruption of the class B, scavenger receptor CD36 protects against atherosclerotic lesion development in mice Academic Article uri icon

Overview

MeSH Major

  • Antigens, CD36
  • Arteriosclerosis
  • Receptors, Immunologic

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.

publication date

  • April 2000

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC300837

PubMed ID

  • 10772649

Additional Document Info

start page

  • 1049

end page

  • 56

volume

  • 105

number

  • 8