Modulation of RAGE expression influences the adhesion of red blood cells from diabetic patients

Article type: Research Article

Authors: Wautier, Marie-Paule | Khodabandehlou, Taraneh | Le Dévéhat, Claude | Wautier, Jean-Luc^{; ;}

Affiliations: Inserm, U 665, Paris F-75015, France | Institut National de la Transfusion Sanguine, Paris, France | Unité de Recherche d'Hémorhéologie CH Nevers, Université Paris 7/Denis Diderot, Paris, France | UFR Médecine, Université Paris 7/Denis Diderot, Paris F-75005, France

Note: [] Corresponding author: J.L. Wautier, Institut National de la Transfusion Sanguine, 6 rue Alexandre Cabanel, 75739 Paris cedex 15, France. Tel.: +33 1 44 49 30 36; Fax: +33 1 43 06 04 83; E-mail: jlwautier@ints.fr.

Abstract: Atherothrombotic complications are frequent in patients with type 2 diabetes. Red blood cells (RBC) from diabetic patients exhibited an increased adhesion which correlated to the extent of vascular complications. In the present study we have investigated the adhesive interactions of RBCs with endothelium, using flow-based assessments. RBCs and endothelial cells were unstimulated or stimulated using respectively adrenaline and TNFα. Adhesion assays were carried-out by drawing the RBC suspension through a glass microcapillary tube precoated by human umbilical vein endothelial cells. These microslides were then incorporated into a controlled flow system equipped with a computerized video-microscopic image analysis. RBCs from diabetic patients bind to endothelial cells and could withstand wall shear stresses above 0.1 Pa. After stimulation by TNFα the adhesion was 1.5-fold higher. Blocking experiments demonstrated that the adhesion was mediated by the receptor for AGE (RAGE). Adrenaline-treated RBCs showed a transient increase in adhesion at low shear stresses. Inflammatory mediators or catecholamine amplifying diabetic RBC adhesion may aggravate endothelial cell damages.

Journal: Clinical Hemorheology and Microcirculation, vol. 35, no. 3, pp. 379-386, 2006