Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1662-1667
doi: 10.1161/hq1001.096625
doi: 10.1161/hq1001.096625
© 2001 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Adhesion of Monocytes to Arterial Endothelium and Initiation of Atherosclerosis Are Critically Dependent on Vascular Cell Adhesion Molecule-1 Gene Dosage
From The Rockefeller University, New York, NY, and the Toronto General Research Institute (M.I.C.), University of Toronto, Toronto, Ontario, Canada.
Correspondence to Jonathan D. Smith, The Rockefeller University, 1230 York Ave, New York, NY 10021. E-mail smithj{at}rockvax.rockefeller.edu
Abstract—— 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.
Key Words: vascular cell adhesion molecule-1 • apolipoprotein E • hypercholesterolemia • gene targeting • monocytes
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