Fig. 6.

SDF-1α-mediated enhancement of platelet activation is primarily TxA₂-dependent and ADP-independent. Washed platelets (2 × 10⁸/mL^− 1) were pre-treated with vehicle control or inhibitors; 10 μM indomethacin (cyclooxygenase) or 1 μM AR-C and 10 μM MRS 2279 (P2Y₁ and P2Y₁₂, respectively) and co-stimulated with threshold doses of collagen and 100 ng/mL^− 1 SDF-1α. For inhibitor treated samples, platelets were stimulated with 2 μg/mL^− 1 collagen (vs. 0.5 μg/mL^− 1 in non-inhibitor treated samples) to induce threshold aggregation responses that were comparable to non-inhibitor treated samples. * in Ai–ii denotes different collagen concentrations. Platelet aggregation with representative traces (Ai–ii), area under the curve analysis (Aiii) and peak ATP secretion (B) were assessed by lumi-aggregometry, with the releasates from aggregated samples analysed for TxB₂ (C). Data are mean ± SEM, n = 5, non-significant (ns), *P < 0.05, **P < 0.01, ***P < 0.001 vs. vehicle, Two-way ANOVA with Bonferroni post-hoc analysis.