Platelet PECAM-1 inhibits thrombus formation in vivo Academic Article uri icon

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abstract

  • Abstract 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.

authors

  • Falati, Shahrokh
  • Patil, Sonali
  • Gross, Peter Lawrence
  • Stapleton, Michelle
  • Merrill-Skoloff, Glenn
  • Barrett, Natasha E
  • Pixton, Katherine L
  • Weiler, Harmut
  • Cooley, Brian
  • Newman, Debra K
  • Newman, Peter J
  • Furie, Barbara C
  • Furie, Bruce
  • Gibbins, Jonathan M

publication date

  • January 15, 2006

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