Effect of different platelet inhibitors and GP IIb/IIIa antagonists on plasma levels of LIGHT. (A) Release of LIGHT from platelets in PRP (after 90 minutes of activation), in the presence of EDTA (5 mM), cytochalasin D (60 μM), or GM 6001 (30 μM) added to PRP 10 minutes after the activation agonist SFLLRN (100 μM), compared to stimulated platelets with solvent added instead of inhibitor. Data are presented as mean ± SEM, n = 5. (B) Release of LIGHT (pg/10⁸ platelets) measured in the extracellular phase after activation of platelets in PRP by SFLLRN (100 μM) from stimulated platelets (•), from platelets preincubated (for 10 minutes) with abciximab (▴; 40 μg/mL), and from platelets obtained from a patient (▪) with Glanzmann thrombasthenia (lacking the aggregation receptor GP IIb/IIIa). Data are presented as mean ± SEM; n = 10, n = 5 and n = 1, respectively. *P < .05 versus no inhibitor (panel A) and versus unstimulated platelets at the same point of time (panel B). (C) Release of LIGHT from platelets in PRP stimulated with 100 μM SFLLRN (for 90 minutes) from patients with unstable angina with (n = 10) and without (n = 10) anti–GP IIb/IIIa therapy. (D) LIGHT in platelet pellets (at baseline) obtained from the same patient groups. Data are presented as mean ± SEM, **P < .01 and ***P < .001 versus patients without anti–GP IIb/IIIa therapy. (E) Release of LIGHT from platelets in PRP after preincubation with aspirin (1 mM) for 20 minutes and stimulation with SFLLRN (100 μM) for 90 minutes. (F) Effect of aspirin (160 mg once a day, for 7 days) on plasma levels of LIGHT in 12 healthy controls.