Figure 2.
Fractalkine-mediated degranulation of rat platelets. (A) P-selectin surface expression in platelets from healthy Wistar-Kyoto rats under basal conditions and following stimulation with recombinant fractalkine (rrCX3C; 1 μg/mL) compared with control samples from the same animals and inhibition by preincubation with either sodium nitroprusside (SNP; 100 μM) or acetyl salicylic acid (ASA; 10 μg/mL) compared with the expression achieved by incubation with ADP (5 μM). (B) Neutralization of recombinant fractalkine by an antagonizing antifractalkine antibody (AF537; 100 μg/mL; 30 min) and inhibition of fractalkine receptor–mediated platelet activation by inhibition of G-protein coupling of the fractalkine-receptor by PTX (0.4 nM; 45 min). (C) P-selectin surface expression in platelets from healthy Wistar-Kyoto rats following stimulation with recombinant fractalkine (rrCX3C; 1 μg/mL) compared with control samples from the same animals in the presence and absence of apyrase (7.5 U/mL). Data are expressed as mean fluorescence ± SEM from 6 separate animals. *P < .01 versus basal; #P < .01 versus rrCX3C; §P < .01 versus ADP.