Figure 4
Figure 4. In vivo analysis of arterial thrombosis in wild-type and IRAGΔ12/Δ12 mice. (A) Thrombus formation in the injured carotid artery of wild-type (WT) and IRAGΔ12/Δ12 mice in the absence or presence of NO (50 μM NO-spermine) or PGI2 (50 μM iloprost) (arrowheads indicate thrombi; arrows, single, adherent platelets). (B) Statistical evaluation of thrombus formation as measured by the size of platelet aggregates (in μm2) Analysis was performed with n = 6 to 9 PBS-, vehicle (NaOH)–, NO- or PGI2-treated WT or IRAG mutant mice. (C) Thrombus formation after infusion of IRAGΔ12/Δ12 or WT platelets into the injured carotid artery of WT or IRAGΔ12/Δ12 mice (recipient), respectively, in the presence of NO (50 μM NO-spermine) (arrowheads indicate thrombi, n = 4). Representative videoclips of thrombus formation in WT or IRAGΔ12/Δ12 mice from panel A in the presence or absence of nitric oxide are available as Videos S1–S4.

In vivo analysis of arterial thrombosis in wild-type and IRAGΔ12/Δ12 mice. (A) Thrombus formation in the injured carotid artery of wild-type (WT) and IRAGΔ12/Δ12 mice in the absence or presence of NO (50 μM NO-spermine) or PGI2 (50 μM iloprost) (arrowheads indicate thrombi; arrows, single, adherent platelets). (B) Statistical evaluation of thrombus formation as measured by the size of platelet aggregates (in μm2) Analysis was performed with n = 6 to 9 PBS-, vehicle (NaOH)–, NO- or PGI2-treated WT or IRAG mutant mice. (C) Thrombus formation after infusion of IRAGΔ12/Δ12 or WT platelets into the injured carotid artery of WT or IRAGΔ12/Δ12 mice (recipient), respectively, in the presence of NO (50 μM NO-spermine) (arrowheads indicate thrombi, n = 4). Representative videoclips of thrombus formation in WT or IRAGΔ12/Δ12 mice from panel A in the presence or absence of nitric oxide are available as Videos S1–S4.

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