Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Palabrica, T. et al.

Leukocyte accumulation promoting fibrin deposition is mediated in vivo by P-selectin on adherent platelets.

The glycoprotein P-selectin is a cell adhesion molecule of stimulated platelets and endothelial cells, which mediates the interaction of these cells with neutrophils and monocytes. It is a membrane component of cell storage granules, and is a member of the selectin family which includes E-selectin and L-selectin. P-selectin recognizes both lineage-specific carbohydrate ligands on monocytes and neutrophils, including the Lewis x antigen, sialic acid, and a protein component. In inflammation and thrombosis, P-selectin may mediate the interaction of leukocytes with platelets bound in the region of tissue injury and with stimulated endothelium. To evaluate the role of P-selectin in platelet-leukocyte adhesion in vivo, the accumulation of leukocytes within an experimental thrombus was explored in an arteriovenous shunt model in baboons. A Dacron graft implanted within an arteriovenous shunt is thrombogenic, accumulating platelets and fibrin within its lumen. These bound platelets express P-selectin. Here we show that antibody inhibition of leukocyte binding to P-selectin expressed on platelets immobilized on the graft blocks leukocyte accumulation and inhibits the deposition of fibrin within the thrombus. These results indicate that P-selectin is an important adhesion molecule on platelets, mediating platelet-leukocyte binding in vivo, that the presence of leukocytes in thrombi is mediated by P-selectin, and that these leukocytes promote fibrin deposition.[1]

References

Leukocyte accumulation promoting fibrin deposition is mediated in vivo by P-selectin on adherent platelets. Palabrica, T., Lobb, R., Furie, B.C., Aronovitz, M., Benjamin, C., Hsu, Y.M., Sajer, S.A., Furie, B. Nature (1992) [Pubmed]

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