CCL1 and the conditioned medium resulting from incubation of Lp(a) with human umbilical vein endothelial cells induce chemotaxis of VSMCs that is inhibited by anti-CCR8 and anti-CCL1. CCL1 (100 ng/mL) or the CM obtained following incubation of DMEM (CM) or Lp(a) (150 μg/mL) (LCM) with HUVECs for 6 hours at 37°C was tested for VSMC chemotaxis as described in “Materials and methods.” Murine monoclonal antibody against CCR8, the isotypic IgG1 control (A), or polyclonal goat anti-CCL1 and the goat IgG control (B), all at a concentration of 1 μg/mL, were also added to the bottom wells of the chemotaxis chamber. (A) Anti-CCR8 significantly inhibited chemotaxis of VSMCs induced by CCL1 and LCM (*P < .00 001). The cell-stimulating activity of LCM was significantly greater than that of CM (P = .005). Inhibition of CM by anti-CCR8 was of borderline significance (P = .05). Neither DMEM nor Lp(a) added to the lower wells of the chemotaxis chamber induced significant VSMC chemotaxis (4.3 ± 1.4 and 7.1 ± 2.2 cells/high power field (hpf), respectively). These findings indicate that CCR8 mediates chemotaxis of VSMCs. (B) Anti-CCL1 significantly inhibited chemotaxis of VSMCs induced by CCL1 and LCM (*P = .007 and **P = .002, respectively). CM was not significantly inhibited by anti-CCL1. The cell-stimulating activity of LCM was significantly greater than that of CM (P = .01). DMEM and Lp(a) alone induced 7.0 ± 3.3 and 11.7 ± 2.6 cells/high power field, respectively. These data demonstrate that the chemotaxis of VSMCs induced by LCM is due to the presence of CCL1. Error bars represent SD.