Thrombospondin from Activated Platelets Promotes Sickle Erythrocyte Adherence to Human Microvascular Endothelial Cells Via CD36 and Integrin Receptors

Adherence of erythrocytes to vascular endothelium likely contributes to the pathophysiology of episodic microvascular occlusion in patients with sickle cell disease (Wick, et al., 1987). In addition, coagulation activation has been reported in sickle patients during complications such as pain episodes (Francis and Johnson, 1991). Since platelets contain adhesion proteins (e.g. von Willebrand factor, thrombospondin and fibrinogen), we investigated whether factors released from activated platelets from sickle patients promote adherence of sickle erythrocytes to human microvascular endothelial cells (MEC) under flow conditions.