Molecular Mechanism of Erythrocyte Adhesion to Endothelium

Molecular Mechanism of Erythrocyte Adhesion to Endothelium

It is the first time that red blood cell interaction to endothelium was explored in several diseases and the molecular basis identified. Vascular complication is the major cause of morbidity and mortality. Coagulation abnormalities and platelet activation were found to participate in thrombosis, however very little was known about the role of Red Blood Cell (RBC). Abnormal RBC adhesion to Endothelial Cells (EC) was first discovered in Sickle Cell Disease (SCD) and in diabetes mellitus. The molecular basis was identified implying adhesion molecules, VCAM, LuBCAM, and laminin in SCD. One year later, in diabetes, it was discovered that vascular complication was correlated to the extent of RBC adhesion to EC. Glycation of RBC band3 mediated the binding to the Receptor RAGE present on EC. Patients with Polycythemia Vera have a high incidence of mesenteric and cerebral vascular complications. RBC adhesion to EC laminin is due to LuBCAM phosphorylation secondary to JAK2 mutation. In Malaria Plasmodium Falciparum infested RBC and induced parasite protein expression, PfEMP 1 which is the ligand for EC. This book was designed to MD, biologists, hematologists, and students.