Figure 2
Figure 2. ILK is required for the up-regulation of integrin αIIbβ3 function. The exposure of integrin αIIbβ3 on the platelet surface was measured by flow cytometry in resting platelets (A; **P ≤ .01), and thrombin-stimulated platelets (B; ***P ≤ .01). Fibrinogen binding was assessed in the ILK-deficient and control (Ctrl) platelets using FITC-labeled fibrinogen and flow cytometry. Platelets were stimulated with either collagen (C; *P ≤ .05) or thrombin (D; ***P ≤ .005) (average reduction of 60% in the KO compared with the WT). Data for fibrinogen binding upon thrombin activation was normalized to account for the reduction in surface receptors (E). All data expressed as mean plus or minus SEM, n = 4.

ILK is required for the up-regulation of integrin αIIbβ3 function. The exposure of integrin αIIbβ3 on the platelet surface was measured by flow cytometry in resting platelets (A; **P ≤ .01), and thrombin-stimulated platelets (B; ***P ≤ .01). Fibrinogen binding was assessed in the ILK-deficient and control (Ctrl) platelets using FITC-labeled fibrinogen and flow cytometry. Platelets were stimulated with either collagen (C; *P ≤ .05) or thrombin (D; ***P ≤ .005) (average reduction of 60% in the KO compared with the WT). Data for fibrinogen binding upon thrombin activation was normalized to account for the reduction in surface receptors (E). All data expressed as mean plus or minus SEM, n = 4.

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