Objectives - The α2/β1 integrin serves as a collagen or collagen/laminin receptor on many cell types, including endothelial cells and platelets. Many studies indicate that the α 2/β1 integrin is a critical mediator of platelet adhesion to collagen. Epidemiologic studies suggest a direct correlation between the genetically determined platelet surface density of the α 2/β1 integrin and the risk of thrombotic diseases, such as myocardial infarction and stroke, in the young, which are well-established complications of atherosclerosis. We have now used the α2β1 integrin-deficient mouse to evaluate the contributions of the α2/β1 integrin to the development of atherosclerosis. Methods and Results - We generated wild-type (α2+/+) or α2/β1 integrin-deficient (α2-/-) mice that were also deficient in the apolipoprotein E (ApoE) gene (ApoE-/-) and compared atherosclerotic lesion development in α2+/+ ApoE-/- and α2-/- ApoE-/- mice that were fed a high-fat, cholesterol-containing diet for 6 or 15 weeks. Total lesional area did not differ significantly between the α 2-null animals and the wild-type animals at either 6 or 15 weeks. Conclusions - Our results suggest that risk for arterial thrombotic disease associated with high-level α2/β1 integrin expression is not attributable to enhanced development of atherosclerosis per se but may rather be a consequence of thrombotic complications at the plaques.
|Number of pages||6|
|Journal||Arteriosclerosis, thrombosis, and vascular biology|
|State||Published - Nov 2003|