Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion

• Published in: Journal of thrombosis and haemostasis Vol. 9; no. 5; pp. 1049 - 1055
• Main Authors: WAUTIER, M.‐P., HÉRON, E., PICOT, J., COLIN, Y., HERMINE, O., WAUTIER, J.‐L.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.2011; Wiley Subscription Services, Inc
• Subjects: adhesion molecules; Adult; Aged; Annexin A5 - chemistry; Cell Adhesion; endothelial cell; Erythrocyte Aggregation; Erythrocytes - cytology; Female; Hematocrit; Humans; Male; Middle Aged; phosphatidylserine; Phosphatidylserines - blood; Phosphatidylserines - chemistry; red blood cell; Retinal Artery - cytology; Retinal Vein Occlusion - blood; retinal vessels; Retinal Vessels - metabolism
• DOI: 10.1111/j.1538-7836.2011.04251.x
• ISSN: 1538-7933; 1538-7836

Background: Retinal vein occlusion (RVO) is a common cause of permanent loss of vision. The pathophysiology is uncertain, although enhanced erythrocyte aggregation and blood hyperviscosity have been observed. Increased red blood cell (RBC) adhesion has been associated with vascular complications in several diseases, such as sickle cell anemia, diabetes mellitus or polycythemia vera. Objectives: To measure RBC adhesion to endothelial cells in RVO and to explore the molecular basis of the adhesion process. Patients and methods: We assessed RBC adhesion to endothelial cells and adhesion molecule expression among 32 patients with RVO. Patients with disease known to alter RBC adhesion were excluded (n = 8), and further investigation was conducted in 20 patients with central retinal vein occlusion (CRVO) and four patients with retinal artery occlusion (RAO), compared with 25 normal subjects. Results: Under static conditions, adhesion of CRVO RBC was increased (135 ± 7 × 102 mm−2) compared with RAO RBC (63 ± 5 × 102 mm−2) (P < 0.01) and normal control RBC (37 ± 3 × 102 mm−2) (P < 0.001). Under flow conditions, CRVO RBC adhered in greater numbers than normal RBC (P < 0.001). Phosphatidylserine (PS) expression on CRVO RBC was 2.4‐fold higher than controls and correlated with RBC adhesion (P = 0.001). In static conditions, specific antibodies against PS receptor and annexin V inhibited RBC adhesion. In flow conditions, the inhibitory effect was in the same range with antibodies but was 2‐fold higher with annexin V. Conclusion: Increased CRVO RBC adhesion is mediated by PS RBC and endothelial PS receptor. This phenomenon may be one of the factors responsible for CRVO.