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

Overview

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 1, 2000

Research

keywords

  • Arteriosclerosis
  • CD36 Antigens
  • Receptors, Immunologic

Identity

PubMed Central ID

  • PMC300837

Scopus Document Identifier

  • 0034101821

Digital Object Identifier (DOI)

  • 10.1172/JCI9259

PubMed ID

  • 10772649

Additional Document Info

volume

  • 105

issue

  • 8