Figure 3
Figure 3. LIMK1 selectively promotes VWF-stimulated platelet TXB2 production and platelet adhesion under shear stress. (A-B) TXB2 production in WT and LIMK1−/− platelets stimulated with: (A) VWF and botrocetin or with botrocetin alone as a control, or (B) collagen or PAR4AP. All data are expressed as mean ± standard error. Statistical significance was determined using the Student t test, **P < .01. (C) Stable adhesion of mepacrine-stained WT and LIMK1−/− platelets to VWF-coated slides under a constant shear rate (800 s−1). The adherent platelets were photographed under a Leica fluorescence microscope. The number of adherent platelets per field in ≥20 randomly selected fields (4 experiments) is shown (mean ± SE). The first, third, and fourth columns are adhesion of WT platelets (with or without pretreatment with the integrin inhibitor RGDS or the cyclooxygenase inhibitor aspirin), and the second and fifth columns are LIMK1−/− platelets (with or without 40 nM U46619).

LIMK1 selectively promotes VWF-stimulated platelet TXB2 production and platelet adhesion under shear stress. (A-B) TXB2 production in WT and LIMK1−/− platelets stimulated with: (A) VWF and botrocetin or with botrocetin alone as a control, or (B) collagen or PAR4AP. All data are expressed as mean ± standard error. Statistical significance was determined using the Student t test, **P < .01. (C) Stable adhesion of mepacrine-stained WT and LIMK1−/− platelets to VWF-coated slides under a constant shear rate (800 s−1). The adherent platelets were photographed under a Leica fluorescence microscope. The number of adherent platelets per field in ≥20 randomly selected fields (4 experiments) is shown (mean ± SE). The first, third, and fourth columns are adhesion of WT platelets (with or without pretreatment with the integrin inhibitor RGDS or the cyclooxygenase inhibitor aspirin), and the second and fifth columns are LIMK1−/− platelets (with or without 40 nM U46619).

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