Figure 7.
The role of PTPN22 role in human platelet function. Washed human platelets were isolated and pretreated with 20 μM LTV-1 (PTPN22 inhibitor) for 1 hour at 37°C followed by analysis of platelet aggregation after stimulation with CRP (0.1 μg/mL) or thrombin (0.02 U/mL) (mean ± standard deviation [SD], n = 3; t test) (A), platelet spreading on collagen or fibrinogen (mean ± SD, n = 3; t test) (scale bar = 10 μm) (B), and clot retraction induced by thrombin (0.8 U/mL) (mean ± SD, n = 3; two-way analysis of variance) (C). (D) PDE5A phosphorylation was also measured in platelets stimulated with CRP 5 μg/mL in the presence or absence of LTV-1 (mean ± SD, n = 3 independent experiments; two-way analysis of variance). **P < .01, ***P < .001.

The role of PTPN22 role in human platelet function. Washed human platelets were isolated and pretreated with 20 μM LTV-1 (PTPN22 inhibitor) for 1 hour at 37°C followed by analysis of platelet aggregation after stimulation with CRP (0.1 μg/mL) or thrombin (0.02 U/mL) (mean ± standard deviation [SD], n = 3; t test) (A), platelet spreading on collagen or fibrinogen (mean ± SD, n = 3; t test) (scale bar = 10 μm) (B), and clot retraction induced by thrombin (0.8 U/mL) (mean ± SD, n = 3; two-way analysis of variance) (C). (D) PDE5A phosphorylation was also measured in platelets stimulated with CRP 5 μg/mL in the presence or absence of LTV-1 (mean ± SD, n = 3 independent experiments; two-way analysis of variance). **P < .01, ***P < .001.

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