Figure 2
Figure 2. Effect of Gα12 on platelet accumulation at the site of vascular injury in live mice. (A) Induced tail-snip blood loss in EC-Gα13−/−;Gα12−/− vs WT mice, measured as Hb concentration accumulating in a saline-filled microfuge tube over the course of 15 minutes. Infusion of purified human vWF (vehicle in WT mice) into the jugular vein of EC-Gα13−/−;Gα12−/− mice induced partial recovery of the hemorrhagic event (n = 3 mice/group). (B) WT and Gα12−/− mice (n = 3) were infused with Dylight 649–conjugated anti-mouse CD42c antibody (0.05 μg/g body weight) through a cannulus placed in a jugular vein. After laser injury, platelet thrombus formation was monitored via real-time intravital microscopy. Representative images of fluorescence associated with platelets (red) over the course of 240 seconds after vascular injury within the context of bright-field arteriolar histology. (C) Median integrated fluorescence intensity of anti-CD42c antibodies (Fplatelets) in 25 thrombi in 3 WT and 3 Gα12−/− mice.

Effect of Gα12 on platelet accumulation at the site of vascular injury in live mice. (A) Induced tail-snip blood loss in EC-Gα13−/−;Gα12−/− vs WT mice, measured as Hb concentration accumulating in a saline-filled microfuge tube over the course of 15 minutes. Infusion of purified human vWF (vehicle in WT mice) into the jugular vein of EC-Gα13−/−;Gα12−/− mice induced partial recovery of the hemorrhagic event (n = 3 mice/group). (B) WT and Gα12−/− mice (n = 3) were infused with Dylight 649–conjugated anti-mouse CD42c antibody (0.05 μg/g body weight) through a cannulus placed in a jugular vein. After laser injury, platelet thrombus formation was monitored via real-time intravital microscopy. Representative images of fluorescence associated with platelets (red) over the course of 240 seconds after vascular injury within the context of bright-field arteriolar histology. (C) Median integrated fluorescence intensity of anti-CD42c antibodies (Fplatelets) in 25 thrombi in 3 WT and 3 Gα12−/− mice.

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