The
selectins are
membrane glycoproteins promoting adhesive events between leukocytes, platelets, and endothelial cells. We have previously demonstrated that platelets roll on
P-selectin expressed on stimulated endothelium. In this study, we wished to examine the function of both the platelet and endothelial
selectins, P- and E-
selectins, in mediating platelet-endothelial interactions during
inflammation. We demonstrate, using intravital microscopic examination of venules inflamed with
tumor necrosis factor-alpha (
TNF-alpha), that resting platelets interact with both P- and E-
selectins and that the leukocyte alpha(1,3)
fucosyltransferases FucT IV and FucT VII do not provide platelets with
selectin ligand activity. We also show that after
thrombin activation of wild-type (+/+) platelets, platelet
P-selectin can mediate interactions on a
TNF-alpha-inducible endothelial
ligand. To evaluate the potential role of platelet
P-selectin in the recruitment of leukocytes to inflammatory sites, we reconstituted the bone marrow of mice deficient in both P- and E-
selectins (P/E-/-) with wild-type (+/+) or
P-selectin-deficient (P-/-) bone marrow containing megakaryocytic precursors. Providing +/+ platelets to P/E-/- mice by
bone marrow transplantation did not rescue the immunodeficient phenotype, suggesting that platelet
P-selectin does not have an active function in the recruitment of leukocytes into inflammatory sites. To participate in inflammatory or
hemostatic responses, platelets may use the endothelial
selectins.