Abstract
Despite clinical and epidemiological studies quantitative and qualitative abnormalities red blood cell (RBC) role in thrombosis has been ignored. Abnormal interaction of RBCs with vascular endothelium has been demonstrated in diabetes mellitus, Polycythemia vera (PV) and retinal vascular occlusion (RVO) after the first description in sickle cell anemia. The molecular basis has been identified. In diabetes mellitus, glycation of RBC band 3 caused the ligation to the receptor for advanced glycation end products (RAGE) present on endothelium. An abnormal Lu/BCAM (CD 239) expression in PV is responsible for the binding to endothelium annexin V. In RVO, RBC phosphatidylserine overexpression mediated the attachment to vascular laminin alpha-5 chain. Red blood cell binding altered the nonthrombotic properties of endothelium leading to thrombosis.
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