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 Blood, 15 July 2006, Vol. 108, No. 2, pp. 510-514.
Prepublished online as a Blood First Edition Paper on February 28, 2006; DOI 10.1182/blood-2005-12-4835.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Reduced thrombus stability in mice lacking the {alpha}2A-adrenergic receptor

Miroslava Pozgajová, Ulrich J. H. Sachs, Lutz Hein, and Bernhard Nieswandt

From the Rudolf Virchow Center, Deutsche Forschungsgemeinschaft (DFG) Center for Experimental Biomedicine, the Institute of Pharmacology and Toxicology, and the Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg, Germany.

Platelet activation plays a central role in hemostasis and thrombosis. Many platelet agonists function through G-protein–coupled receptors. Epinephrine activates the {alpha}2A-adrenergic receptor ({alpha}2A) that couples to Gz in platelets. Although {alpha}2A was originally cloned from platelets, its role in thrombosis and hemostasis is still unclear. Through analysis of {alpha}2A-deficient mice, variable tail bleeding times were observed. In vitro, epinephrine potentiated activation/aggregation responses of wild-type but not {alpha}2A-deficient platelets as determined by flow cytometry and aggregometry, whereas perfusion studies showed no differences in platelet adhesion and thrombus formation on collagen. To test the in vivo relevance of {alpha}2A deficiency, mice were subjected to 3 different thrombosis models. As expected, {alpha}2A-deficient mice were largely protected from lethal pulmonary thromboembolism induced by the infusion of collagen/epinephrine. In a model of FeCl3-induced injury in mesenteric arterioles, {alpha}2A–/– mice displayed a 2-fold increase in embolus formation, suggesting thrombus instability. In a third model, the aorta was mechanically injured, and blood flow was measured with an ultrasonic flow probe. In wild-type mice, all vessels occluded irreversibly, whereas in 24% of {alpha}2A-deficient mice, the initially formed thrombi embolized and blood flow was reestablished. These results demonstrate that {alpha}2A plays a significant role in thrombus stabilization.


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