Monocyte chemoattractant protein?1 (MCP-1) is a well known determinant of arteriogenesis, regulating recruitment and activation of monocytes as a prerequisite for the remodelling of arterioles which run in parallel to an occluded artery. In vivo studies employing a mouse ear artery ligation model as well as the classical hind limb ischemia model confirmed a strong MCP-1 up-regulation in the collateral arterioles during the initial phase of arteriogenesis. As shear stress and circumferential wall strain are supposed to initiate the arteriogenic remodelling process we investigated to what extent these biomechanical parameters affect the expression of MCP-1. Previous in vitro experiments revealed that cyclic stretch but not shear stress up-regulated MCP-1 in endothelial as well as in smooth muscle cells. Furthermore, paracrine interaction of endothelial and smooth muscle cells significantly enhances cyclic stretch induced MCP-1 expression. To more closely mimic the biomechanical load of the vessel wall during arteriogenesis we established a perfusion system using isolated mouse mesenteric arteries. Gene expression studies revealed that smooth muscle cells significantly up-regulate MCP-1 even after short term perfusion under arteriogenic conditions. Taken together, our results suggest that MCP-1 expression is indeed up-regulated in response to cyclic stretch and that this plays a critical role during the onset of arteriogenesis.