Chemokines induce matrix metalloproteinase-2 through activation of epidermal growth factor receptor in arterial smooth muscle cells.

Objective: Matrix metalloproteinases (MMP) are critical to smooth muscle cell (SMC) migration in vivo. MMP-2 dysregulation has been implicated in the pathogenesis of abnormal arterial remodeling, aneurysm formation, and atherosclerotic plaque structure and stability. The chemokine receptors CCR3 and CXCR4 are present and functional on SMC and are up-regulated in vascular diseases such as atherosclerosis.

MCP-1-dependent signaling in CCR2(-/-) aortic smooth muscle cells.

Monocyte chemoattractant protein-1 (MCP-1, CCL2) is a mediator of inflammation that has been implicated in the pathogenesis of a wide variety of human diseases. CCR2, a heterotrimeric G-coupled receptor, is the only known receptor that functions at physiologic concentrations of MCP-1. Despite the importance of CCR2 in mediating MCP-1 responses, several recent studies have suggested that there may be another functional MCP-1 receptor.

Chemokine receptors in vascular smooth muscle.

Atherosclerosis is considered to be an inflammatory disease. Chemokines are low-molecular-weight proteins that exert their effects, in part, through mediating leukocytic infiltration into the vessel wall. Recently, studies have determined that chemokines and their receptors are present, and function on other cellular components comprising the arterial wall, such as the endothelium and vascular smooth muscle.