Figure 6
Figure 6. Enhanced activation by collagen in Pf4-Loxtg/tg platelets is mediated by integrin α2β1. (A) Platelet adhesion and spreading assay of WT and Pf4-Loxtg/tg platelets preincubated with antibodies against integrin α2 or isotype control (10 μg/mL). Results are the average ± SD of 3 independent experiments, with 1 mouse per group in each experiment. No statistically significant difference was detected between “no antibody” and “isotype” samples in either the WT or the Pf4-Loxtg/tg group. (B) Flow cytometric analysis of P-selectin (CD62p) expression after stimulation with CRP-XL in platelets from WT (n = 4) and Pf4-Loxtg/tg (n = 4) mice. Data are represented as average ± SD. (C) Platelet adhesion and spreading assay on GFOGER (50 μg/mL); the average ± SD of the number of adhered and spread platelets is shown. (D) Representative image of platelet adhesion and spreading assay on GFOGER. *P < .05, **P < .001.

Enhanced activation by collagen in Pf4-Loxtg/tg platelets is mediated by integrin α2β1. (A) Platelet adhesion and spreading assay of WT and Pf4-Loxtg/tg platelets preincubated with antibodies against integrin α2 or isotype control (10 μg/mL). Results are the average ± SD of 3 independent experiments, with 1 mouse per group in each experiment. No statistically significant difference was detected between “no antibody” and “isotype” samples in either the WT or the Pf4-Loxtg/tg group. (B) Flow cytometric analysis of P-selectin (CD62p) expression after stimulation with CRP-XL in platelets from WT (n = 4) and Pf4-Loxtg/tg (n = 4) mice. Data are represented as average ± SD. (C) Platelet adhesion and spreading assay on GFOGER (50 μg/mL); the average ± SD of the number of adhered and spread platelets is shown. (D) Representative image of platelet adhesion and spreading assay on GFOGER. *P < .05, **P < .001.

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