Figure 1.
Figure 1. Angiostatin interferes with leukocyte adhesion. The adhesion of PMA-stimulated THP-1 cells to immobilized vitronectin (A), fibrinogen (B), ICAM-1 (C), fibronectin (D), or VCAM-1 (E) in the absence or presence of increasing concentrations of K1-4 (▴), K1-3 (▪), or K4 (○) in the soluble phase is shown. (F) The adhesion of PMA-stimulated human neutrophils to immobilized fibrinogen (▪) or immobilized fibronectin (▦]) is shown in the absence (–) or presence of inhibitory mAb (anti-Mac-1 or anti-β1, respectively, each 20 μg/mL), K1-4, K1-3, K4 (each 1000 nM), or a combination of K1-3 and K4, as indicated. Cell adhesion is represented as absorbance at 590 nm. All data are mean ± SD (n = 3) of a typical experiment; similar results were obtained in 3 separate experiments.

Angiostatin interferes with leukocyte adhesion. The adhesion of PMA-stimulated THP-1 cells to immobilized vitronectin (A), fibrinogen (B), ICAM-1 (C), fibronectin (D), or VCAM-1 (E) in the absence or presence of increasing concentrations of K1-4 (▴), K1-3 (▪), or K4 (○) in the soluble phase is shown. (F) The adhesion of PMA-stimulated human neutrophils to immobilized fibrinogen (▪) or immobilized fibronectin (▦]) is shown in the absence (–) or presence of inhibitory mAb (anti-Mac-1 or anti-β1, respectively, each 20 μg/mL), K1-4, K1-3, K4 (each 1000 nM), or a combination of K1-3 and K4, as indicated. Cell adhesion is represented as absorbance at 590 nm. All data are mean ± SD (n = 3) of a typical experiment; similar results were obtained in 3 separate experiments.

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