Fig. 4.
Murine monoclonal antibody against CCR8 inhibits chemotaxis of HUVECs in response to I-309, vMIP-I, and LCM.
I-309, vMIP-I, or SDF-1 (100 ng/mL each) was used to induce endothelial chemotaxis. The HUVECs were used without treatment (No treatment) or were incubated 30 minutes with 1 μg murine monoclonal antibody against CCR8 (Mab > CCR8), an isotype monoclonal IgG1 control (IgG1), or with a murine monoclonal antibody against CCR2 (isotype IgG1), the MCP-1 receptor (Mab > CCR2). The CM obtained following incubation of Lp(a) (150 μg/mL) with HUVECs for 6 hours (LCM) was also tested using HUVECs from a different donor. These cells had lower background activity when tested using medium 199 (Control). The monoclonal anti-CCR8 inhibited endothelial transmigration stimulated by I-309, vMIP-I, and LCM, but did not inhibit migration in response to SDF-1 (*P < .001). Neither the control murine immunoglobulin nor the monoclonal anti-CCR2 inhibited endothelial chemotaxis in response to the 3 chemokines tested. hpf, high power field.