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(American Journal of Pathology. 2000;157:75-81.)
© 2000 American Society for Investigative Pathology

Short Communications

PECAM-1 (CD31) Expression Modulates Bleeding Time in Vivo

Sepi Mahooti*, Donnasue Graesser*, Sonali Patil{dagger}, Peter Newman{dagger}, Gordon Duncan{ddagger}, Tak Mak{ddagger} and Joseph A. Madri*

From the Department of Pathology,*
Yale University School of Medicine, New Haven, Connecticut; the Blood Research Institute,{dagger}
Blood Center of Southeastern Wisconsin, Milwaukee, Wisconsin; and the AMGEN Institute,{ddagger}
University of Toronto, Toronto, Ontario, Canada

PECAM-1 is a 130-kd member of the Ig superfamily present on endothelial cells, platelets, polymorphonuclear leukocytes, monocytes, and lymphocytes. Its expression begins early in development and persists through adulthood. PECAM-1 functions as an adhesion and signaling molecule between adjacent endothelial cells and between endothelial cells and circulating blood elements. Antibodies directed against PECAM-1 have been shown to affect angiogenesis, endothelial cell migration, and polymorphonuclear leukocyte transmigration. Furthermore, its dimerization is associated with the modulation of integrin affinity. Antibody inhibition studies suggest that PECAM-1 plays a role in modulating thrombosis; however, recent in vitro aggregation studies performed on platelets harvested from PECAM-1-deficient mice revealed no abnormalities. In this report we demonstrate prolonged in vivo bleeding times in PECAM-1-deficient mice. This abnormality was not corrected when wild-type hematopoietic precursors were engrafted into marrow-ablated PECAM-1-deficient mice. Furthermore, normal bleeding times were observed when marrow-ablated wild-type mice were engrafted with hematopoietic precursors harvested from PECAM-1-deficient mice. These studies are consistent with a role for PECAM-1 in modulating thrombosis in the vasculature, which is potentially mediated by endothelial cell PECAM-1 expression.




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