Regulation of cell migration in atherosclerosis.

Abstract

In response to vascular injury, monocytes and smooth muscle cells migrate to the intimal space, resulting in the formation of atherosclerotic and restenotic lesions. Several different growth factors and cytokines have been identified as mediators of cellular migration in the development of neointimal lesions. The principle mediator of monocyte adhesion and recruitment to the injured vascular wall is monocyte chemotactic protein-1. Moreover, recent studies have demonstrated that the atherogenic properties of angiotensin II are due to its ability to induce monocyte chemotactic protein-1 and promote monocyte migration to the vascular wall. Ligand-induced activation of receptor tyrosine kinases are the principle mechanism for smooth muscle cell migration following vascular injury. The signaling pathways mediating receptor-tyrosine kinase-induced migration of smooth muscle cells are also discussed.