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Blood, 15 January 2006, Vol. 107, No. 2, pp. 535-541.
Prepublished online as a Blood First Edition Paper on September 15, 2005; DOI 10.1182/blood-2005-04-1512.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Platelet PECAM-1 inhibits thrombus formation in vivo
Shahrokh Falati,
Sonali Patil,
Peter L. Gross,
Michelle Stapleton,
Glenn Merrill-Skoloff,
Natasha E. Barrett,
Katherine L. Pixton,
Harmut Weiler,
Brian Cooley,
Debra K. Newman,
Peter J. Newman,
Barbara C. Furie,
Bruce Furie, and
Jonathan M. Gibbins
From the Center for Hemostasis and Thrombosis Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; Blood Research Institute, Blood Center of Southeastern Wisconsin, Milwaukee, WI; School of Biological Sciences, The University of Reading, Reading, Berkshire, United Kingdom; and Departments of Physiology, Orthopaedics, Microbiology, Pharmacology, and Cellular Biology, Medical College of Wisconsin, Milwaukee, WI.
Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a cell surface glycoprotein receptor expressed on a range of blood cells, including platelets, and on vascular endothelial cells. PECAM-1 possesses adhesive and signaling properties, the latter being mediated by immunoreceptor tyrosine-based inhibitory motifs present on the cytoplasmic tail of the protein. Recent studies in vitro have demonstrated that PECAM-1 signaling inhibits the aggregation of platelets. In the present study we have used PECAM-1–deficient mice and radiation chimeras to investigate the function of this receptor in the regulation of thrombus formation. Using intravital microscopy and laser-induced injury to cremaster muscle arterioles, we show that thrombi formed in PECAM-1–deficient mice were larger, formed more rapidly than in control mice, and were more stable. Larger thrombi were also formed in control mice that received transplants of PECAM-1–deficient bone marrow, in comparison to mice that received control transplants. A ferric chloride model of thrombosis was used to investigate thrombus formation in carotid arteries. In PECAM-1–deficient mice the time to 75% vessel occlusion was significantly shorter than in control mice. These data provide evidence for the involvement of platelet PECAM-1 in the negative regulation of thrombus formation.
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