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Updated: May 19, 2026

Quantitation of Endothelial Cell Adhesiveness In Vitro
10:24

Quantitation of Endothelial Cell Adhesiveness In Vitro

Published on: June 18, 2015

Molecular basis of erythrocyte adhesion to endothelial cells in diseases

Jean-Luc Wautier1, Marie-Paule Wautier

  • 1Université Denis Diderot, Paris, France. jlwautier@ints.fr

Clinical Hemorheology and Microcirculation
|September 4, 2012
PubMed

Red blood cell (RBC) adhesion to endothelium can be studied in static and flow conditions. Increased RBC adhesion was first described in sickle cell disease. Several molecules were shown to be involved in this phenomenon: VCAM-1, α4β1, Lu/BCAM, ICAM-4. In malaria, Plasmodium falciparum erythrocyte membrane protein1 binds to ICAM-1, PECAM-1 and facilitates the parasite dissemination. In diabetes mellitus augmented RBC adhesion is correlated to the severity of vascular complications. Glycated RBC band3 reacts with the endothelial Receptor for Advanced Glycation End products (RAGE). RAGE engagement induced endothelial cell dysfunction. In patients with Polycythemia Vera (PV), the most frequent myeloproliferative disorder, constitutive phosphorylation of RBC Lu/BCAM is responsible for an increased adhesion to endothelial cell laminin. Retinal vein occlusion (RVO) is a common cause of permanent visual loss. Spontaneous growth of erythroid precursors was observed in more than 25% of patients. RBC adhesion was enhanced and correlated to phosphatidyl serine (PS) expression on RBC. Anti-PS receptor blocked RVO RBC adhesion indicating that the counterpart of RBC PS is PS endothelial cell receptor. Erythrocyte adhesion is mediated by different molecule abnormalities in different diseases but is associated to a higher risk of thrombosis and vascular complications.

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