Fig. 2.
Fig. 2. In vitro adhesion assays between cultured EC and peripheral blood PMN cells. EC were treated (▨) or not (▪) with GAS6 (1 μg/mL) and fluorescein-labeled PMN were then seeded on EC in the presence and absence of PMA (10−7 mol/L), PAF (10−7 mol/L), thrombin (2 U/mL), IL-8 (10−8 mol/L), IL-1β (10 ng/mL), TNF-α (10 ng/mL), FMLP (10-6 mol/L). Relative adhesion shows that PMA, PAF, thrombin, IL-8, IL-1β, TNF-α, and FMLP strikingly increased PMN adhesion to EC. GAS6 significantly inhibited the effect mediated by PMA, PAF, thrombin, IL-1β, and TNF-α, but not that mediated by IL-8 and FMLP. By contrast, GAS6 did not affect PMN adhesion to untreated EC. Results are expressed as relative adhesion percent and represent the mean ± SD from five to eight experiments. Asterisks mark values that are significantly different from the respective control (P < .05) and 100% relative adhesion (bold horizontal line) corresponds to an absolute adhesion of 13 ± 3 cells/microscope field.

In vitro adhesion assays between cultured EC and peripheral blood PMN cells. EC were treated (▨) or not (▪) with GAS6 (1 μg/mL) and fluorescein-labeled PMN were then seeded on EC in the presence and absence of PMA (10−7 mol/L), PAF (10−7 mol/L), thrombin (2 U/mL), IL-8 (10−8 mol/L), IL-1β (10 ng/mL), TNF-α (10 ng/mL), FMLP (10-6 mol/L). Relative adhesion shows that PMA, PAF, thrombin, IL-8, IL-1β, TNF-α, and FMLP strikingly increased PMN adhesion to EC. GAS6 significantly inhibited the effect mediated by PMA, PAF, thrombin, IL-1β, and TNF-α, but not that mediated by IL-8 and FMLP. By contrast, GAS6 did not affect PMN adhesion to untreated EC. Results are expressed as relative adhesion percent and represent the mean ± SD from five to eight experiments. Asterisks mark values that are significantly different from the respective control (P < .05) and 100% relative adhesion (bold horizontal line) corresponds to an absolute adhesion of 13 ± 3 cells/microscope field.

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