Figure 1.
AnxA1Ac2-26 rescues enhanced cerebral thrombus formation. STM and control mice were subjected to light/dye-induced thrombosis with intravenous infusion of 10 mg/kg 5% FITC-dextran followed by photoactivation of cerebral microvessels. (A-D) Images of onset (start of platelet aggregation) and cessation (complete stop of flow for ≥30 seconds) of thrombus formation in control mice and STM. Bars represent 20 μm. The mice were treated with vehicle (saline), AnxA1Ac2-26 (100 μg per mouse), AnxA1Ac2-26+Boc2 (100 μg per mouse + 10 μg per mouse), or AnxA1Ac2-26+WRW4 (100 μg per mouse + 55 μg per mouse), and subjected to light/dye-induced thrombosis, and time of flow cessation (minutes) was quantified in cerebral (E) arterioles and (F) venules. Data are means ± SEM (6-7 mice per group). ***P < .001; ****P < .0001 vs controls. $$$P < .001; $ $ $ $P < .0001 vs STM controls. ΔΔP < .01; ΔΔΔP < .001 vs STM+AnxA1Ac2-26–treated mice.

AnxA1Ac2-26 rescues enhanced cerebral thrombus formation. STM and control mice were subjected to light/dye-induced thrombosis with intravenous infusion of 10 mg/kg 5% FITC-dextran followed by photoactivation of cerebral microvessels. (A-D) Images of onset (start of platelet aggregation) and cessation (complete stop of flow for ≥30 seconds) of thrombus formation in control mice and STM. Bars represent 20 μm. The mice were treated with vehicle (saline), AnxA1Ac2-26 (100 μg per mouse), AnxA1Ac2-26+Boc2 (100 μg per mouse + 10 μg per mouse), or AnxA1Ac2-26+WRW4 (100 μg per mouse + 55 μg per mouse), and subjected to light/dye-induced thrombosis, and time of flow cessation (minutes) was quantified in cerebral (E) arterioles and (F) venules. Data are means ± SEM (6-7 mice per group). ***P < .001; ****P < .0001 vs controls. $$$P < .001; $ $ $ $P < .0001 vs STM controls. ΔΔP < .01; ΔΔΔP < .001 vs STM+AnxA1Ac2-26–treated mice.

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