Influence of angiostatin on neutrophil–endothelial cell interactions. (A) PMA-stimulated adhesion of human neutrophils to endothelial cells is shown in the absence (–) or presence of blocking mAb to β2-integrin, β1-integrin, Mac-1, ICAM-1 (each antibody at 20 μg/mL), K1-4, K1-3, K4, or a combination of K4 with K1-3 (each angiostatin form at 1000 nM). (B) PMA-stimulated adhesion of human neutrophils to endothelial cells is shown in the absence or presence of increasing concentrations of K1-4 (▴), K1-3 (▪), or K4 (○). Cell adhesion is represented as percentage of adherent cell to total added cells. (C) The trans-endothelial migration of human neutrophils in response to 50 ng/mL MCP-1 is shown in the absence (–) or presence of mAb to Mac-1, mAb to β1-integrin (each antibody at 20 μg/mL), K1-4, K1-3, K4, or a combination of K4 with K1-3 (each angiostatin form at 1000 nM). (D) The trans-endothelial migration of human neutrophils in response to 50 ng/mL MCP-1 is shown in the absence or presence of increasing concentrations of K1-4 (▴), K1-3 (▪), or K4 (○). Transmigration is presented as percent of control (only MCP-1, in the absence of competitor). Data are mean ± SD (n = 3) of a typical experiment, similar results were obtained in 3 separate experiments. *P < .001, compared with control.