Figure 5.
BDNF-induced aggregation activates a kinase-dependent pathway. (A) BDNF-induced platelet aggregation in the presence of TrkB kinase domain inhibitors (cyclotraxin B 50 µM and GNF5837 1 µM and 30 µM) as well as broad-spectrum kinase inhibitors (K252a 10 µM and PP2 10 µM). (B) Collagen at 1 µg/mL was used as control (n = 5). Repeated-measures ANOVA, P < .0001; compared with BDNF: no inhibition observed with cyclotraxin B 50 µM and GN5837 1 µM, P > .05; inhibition of BDNF with GNF5837 30 µM, P = .0025; inhibition with K252a 10 µM, P = .004; and inhibition with PP2 10 µM, P = .001. (C) BDNF-induced aggregation in the presence of SFK inhibitors (PRT318 10 µM and dasatinib 10 µM; n = 5). (D) Collagen at 1 µg/mL was used as control (n = 5). Repeated-measures ANOVA, P = .23; inhibition of BDNF with dasatinib 10 µM, P = .34; inhibition with PRT318 10 µM, P = .20. Data are presented as median and IQR.

BDNF-induced aggregation activates a kinase-dependent pathway. (A) BDNF-induced platelet aggregation in the presence of TrkB kinase domain inhibitors (cyclotraxin B 50 µM and GNF5837 1 µM and 30 µM) as well as broad-spectrum kinase inhibitors (K252a 10 µM and PP2 10 µM). (B) Collagen at 1 µg/mL was used as control (n = 5). Repeated-measures ANOVA, P < .0001; compared with BDNF: no inhibition observed with cyclotraxin B 50 µM and GN5837 1 µM, P > .05; inhibition of BDNF with GNF5837 30 µM, P = .0025; inhibition with K252a 10 µM, P = .004; and inhibition with PP2 10 µM, P = .001. (C) BDNF-induced aggregation in the presence of SFK inhibitors (PRT318 10 µM and dasatinib 10 µM; n = 5). (D) Collagen at 1 µg/mL was used as control (n = 5). Repeated-measures ANOVA, P = .23; inhibition of BDNF with dasatinib 10 µM, P = .34; inhibition with PRT318 10 µM, P = .20. Data are presented as median and IQR.

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