Hyperhomocysteinemia (HHcy), as an independent risk factor of atherosclerosis, facilitates endothelial dysfunction and activation of vascular smooth muscle cells (VSMCs).However, little is known about the crosstalk between endothelial cells (ECs) and VSMCs under HHcy.We investigated whether homocysteine (Hcy) activates VSMCs by aberrant secretion ofmitogen platelet-derived growth factors (PDGFs) from ECs in human and in mice.In this study, we found that increased Hcy level did not affect VSMC activity in 24 hrs until the concentration reached 500 μM.