Key result
VCAM-1 deficiency reduces monocyte adherence and fatty streak formation in a gene-dosage-dependent manner.
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- Vascular cell adhesion molecule-1 (VCAM-1/Vcam1) is a cytokine-inducible member of the immunoglobulin gene superfamily that is expressed by arterial endothelial cells in regions predisposed to atherosclerosis and at borders of atherosclerotic plaques. To determine whether VCAM-1 expression regulates atherosclerotic lesion formation, we crossed Vcam1 domain 4-deficient (D4D) mice, which partially circumvent the embryonic lethality of Vcam1 null mice, with apolipoprotein E null (Apoe(-/-)) mice, which spontaneously develop hypercholesterolemia and atherosclerosis. In the Apoe(-/-) background, mice homozygous for the Vcam1 D4D allele had markedly reduced arterial VCAM-1 expression, monocyte adherence in the aortic root, and fatty streak formation. Heterozygous Vcam1 D4D mice revealed a Vcam1 gene-dosage effect and had intermediate, yet significant, reductions in these parameters. Our data demonstrate that VCAM-1 plays a pivotal role in the initiation of atherosclerosis in Apoe(-/-) mice.
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Dansky et al. (2001) studied Atherosclerosis. Vcam1 domain 4-deficient (D4D) allele vs. Wild-type Vcam1 allele was evaluated on Arterial VCAM-1 expression, monocyte adherence in the aortic root, and fatty streak formation. Homozygous and heterozygous Vcam1 D4D deficiency in Apoe(-/-) mice significantly reduced arterial VCAM-1 expression, monocyte adherence, and fatty streak formation in a gene-dosage dependent manner.
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