Shear stress-stimulated endothelial cells induce smooth muscle cell chemotaxis via platelet-derived growth factor-BB and interleukin-1α

One difficulty in the pharmacologic treatment of atherosclerosis or neointimal hyperplasia leading to restenosis is the multiplicity of activated pathways and thus potential treatment targets. This study demonstrates that shear stress, a hemodynamic force that may be a biologically relevant stimulus to induce vascular pathology, stimulates endothelial cells to secrete PDGF-BB and IL-1α. Both of these mediators stimulate the SMC ERK1/2 pathway to induce migration, a critical event in the pathogenesis of atherosclerosis and neointimal hyperplasia. Therefore, this study suggests a relevant common target pathway in SMC that is amenable to manipulation for clinical treatment.