Figure 4.
Figure 4. Inhibition of αIIbβ3 abrogates platelet adhesion and aggregate formation in β1-null mice. (A) Fluorescent wild-type or β1-null platelets were preincubated with 50 μg/mL anti-αIIbβ3 (JON/A F(ab)2 fragments) and injected into recipient mice of the same genotype. Platelet adhesion and aggregate formation following vascular injury were determined by intravital video fluorescence microscopy. The left and right graphs summarize platelet adhesion and aggregate formation, respectively, with and without αIIbβ3 inhibition. The results are presented as mean ± SEM of 7 experiments per group. (B) The photomicrographs show representative in vivo fluorescence microscopy images illustrating platelet adhesion 3 minutes after injury in wild-type and β1-null mice in the presence of anti-αIIbβ3.

Inhibition of αIIbβ3 abrogates platelet adhesion and aggregate formation in β1-null mice. (A) Fluorescent wild-type or β1-null platelets were preincubated with 50 μg/mL anti-αIIbβ3 (JON/A F(ab)2 fragments) and injected into recipient mice of the same genotype. Platelet adhesion and aggregate formation following vascular injury were determined by intravital video fluorescence microscopy. The left and right graphs summarize platelet adhesion and aggregate formation, respectively, with and without αIIbβ3 inhibition. The results are presented as mean ± SEM of 7 experiments per group. (B) The photomicrographs show representative in vivo fluorescence microscopy images illustrating platelet adhesion 3 minutes after injury in wild-type and β1-null mice in the presence of anti-αIIbβ3.

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