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(Circulation Research. 1999;84:1353-1355.)
© 1999 American Heart Association, Inc.

Editorial

Monocyte Rolling in Early Atherogenesis

Vital Role in Lesion Development

David J. Lefer, D. Neil Granger

From the Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, La.

Correspondence to David J. Lefer, PhD, Department of Molecular and Cellular Physiology, LSU Medical Center, 1501 Kings Hwy, Shreveport, LA 71130. E-mail dlefer@lsumc.edu

Key Words: monocyte • gene-targeted mice • hypercholesterolemia • cell adhesion molecule

The process of atherosclerotic lesion formation represents a complex interaction of a number of circulating blood cells with cells that reside within the arterial wall. Understanding the cellular mechanisms involved in this process is vital for the development of novel therapeutic strategies for prevention and treatment of coronary and carotid occlusive disease. In this issue of Circulation Research, Ramos and colleagues¹ describe a novel in vitro model system for visualization and quantification of mononuclear cell rolling in large arteries that are prone to development of atherosclerotic lesions in apolipoprotein E (ApoE)–deficient mice. This novel model system was used to define the contribution of different adhesion molecules to monocyte rolling along atherosclerotic lesions. Their findings are important and should be considered relative to the existing body of published data on leukocyte-endothelial cell interactions in atherosclerosis.

Cell Adhesion Molecules and Atherogenesis

Data generated from animal models of hypercholesterolemia and atherosclerosis suggest that circulating leukocytes (ie, monocytes) contribute to the development of atherosclerotic lesions.^{2 3} Previous studies have demonstrated that the expression of both leukocyte and endothelial cell adhesion molecules (CAMs) is enhanced in the setting of hypercholesterolemia.^{4 5 6 7} Furthermore, atherosclerotic lesions in both animals and humans are a rich source of several endothelial CAMs, including P-selectin, intracellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1).^{8 9 10 11} More recently, gene-targeted mice that are deficient in leukocyte (CD18) or endothelial (P-selectin or ICAM-1) CAMs have been placed on a high-fat diet and the extent of atherosclerosis compared with that produced in their wild-type counterparts placed on the same diet.¹² . . . [Full Text of this Article]

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