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E. Heron, M.-P. Wautier, J. Picot, J.-F. Girmens, M. Paques, Y. Colin, O. Hermine, J.-L. Wautier; Red Blood Cell Adhesion to Vascular Endothelial Cells: A Culprit for Central Retinal Vein Occlusion. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3565.
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We previously observed in vitro endogenous erythroid colony formation in patients with central retinal vein occlusion (CRVO) (E. Héron et al., Ophthalmology 2007), suggesting that red blood cell (RBC) abnormalities may play a role in this condition. In the present study we explored the adhesion of RBC to endothelial cells in CRVO patients, since increased RBC adhesion has been associated with other vaso-occlusive diseases such as sickle cell anemia, diabetes mellitus or polycythemia vera.
Seventeen patients with CRVO, 9 males, aged 21-85 years, all free from the diseases previously associated with increased RBC adhesion, were compared to 13 healthy controls. RBC adhesion to cultured human endothelial cells (ECs) was measured by validated techniques under static conditions and in a flow system using video-microcopy at a range of perfusion pressure from 0.03 Pa to 0.3 Pa. RBC membrane adhesion molecules and phosphatidylserine (PS) exposure were determined by flow cytometry.
In static conditions CRVO patients had an increased RBC adhesion to ECs compared to controls, 140.5±9.6 vs 35.9±3.6 RBCx102/mm2 (P<0.001). RBC adhesion was also enhanced 2- to 3 fold in flow conditions. PS exposure was significantly higher in CRVO RBC (2.1±0.2% positive cells) than in normal RBC (0.6±0.05%, p<0.001). Antibodies directed against the PS receptor present on endothelial cells inhibited RBC adhesion up to 60%.
CRVO patients show increased RBC adhesion to human endothelial cells, mediated by enhanced PS exposure on RBC. This phenomenon may participate in the vascular occlusion mechanism of CRVO.
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