Objective: There is a growing body of evidence that endothelial cells assume an inflammatory phenotype in sickle cell disease. The authors determined whether (1) the expression of E- and P-selectin differs between sickle cell transgenic (βS) mice and their wild-type counterparts, and (2) blood platelets and/or neutrophils contribute to the altered selectin expression. Methods: Expression of E- and P-selectin was measured in different regional vascular beds of wild-type and βS mice (with or without thrombocytopenia) or nueutropenia) using the dual radiolabeled monoclonal antibody technique. Results: Constitutive expression of P-selectin was significantly increased in the heart, lungs, small bowel, large bowel, and penis of βS versus WT mice. While thrombocytopenia reduced P-selectin expression in the small bowel and penis of βS mice, neutropenia was associated with a reduction in P-selectin expression only in the penis. E-selectin expression was not significantly elevated in any vascular bed except the penis of β S Mice. Conclusions: Sickle cell disease promotes an increased P-selectin expression in several vascular beds. An accumulation of platelets may be explain the increased P-selectin expression observed in some vascular beds.
- Endothelial cell adhesion molecules
- Leukocyte adhesion
- Platelet adhesion
- Sickle cell disease