Molecular basis of sickle cell-endothelial cell interactions

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Abstract
Adherence of sickle erythrocytes to microvascular endothelium is posited to initiate or contribute to sickle cell vaso-occlusive pain episodes. Adherence and occlusion in vivo may depend on hemodynamics interacting with plasma, erythrocyte, and endothelial cell factors. Four receptor-mediated adherence pathways have been described to date: adherence mediated by high molecular weight von Willebrand factor multimers bridging glycoprotein Ib-like and integrin receptors on sickle cells and similar receptors on endothelial cells; thrombo-spondin bridging CD36 on sickle reticulocytes and the αvβ3 integrin on large-vessel endothelial cells or αvβ3 and CD36 on microvascular endothelium; binding of sickle reticulocyte α4β1 receptors to vascular cell adhesion molecule 1 expressed on endothelial cells stimulated by cytokine or double-stranded RNA viruses; and binding of sickle cells to endothelial cell-associated fibronectin via sickle reticulocyte α4β1 activated by phorbol ester or interleukin-8. The significance of these adherence pathways in sickle cell vaso-occlusion is discussed.

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