Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion
Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion
复制标题
DOI：
10.1111/j.1538-7836.2011.04251.x
复制
发表时间：
2011-05-01
影响因子：
10.4
通讯作者：
Wautier, J. -L.
中科院分区：
文献类型：
--
作者：
Wautier, M. -P.;Heron, E.;Wautier, J. -L.
背景：视网膜静脉阻塞(RVO)是导致永久性失明的常见原因。虽然已经观察到红细胞聚集增强和血液高粘滞性，但其病理生理尚不确定。红细胞(RBC)粘附性增加与多种疾病的血管并发症有关，如镰状细胞性贫血、糖尿病或真性红细胞增多症。目的：检测RVO中RBC与内皮细胞的黏附，探讨RVO黏附过程的分子基础。患者和方法：我们评估了32例RVO患者的RBC与内皮细胞的黏附和黏附分子的表达。排除已知RBC黏附改变的患者(n=8)，对20例视网膜中央静脉阻塞(CRVO)和4例视网膜动脉阻塞(RAO)患者进行进一步研究，并与25例正常人进行比较。结果：在静态条件下，CRVO红细胞的黏附性(135+/-7×10(2)mm(-2))明显高于RAO红细胞(63+/-5×10(2)mm(-2))(P<0.01)和正常对照红细胞(37+/-3×10(2)mm(-2))(P<；0.001)。在流动条件下，CRVO红细胞比正常红细胞黏附数量更多(P<；0.001)。CRVO患者红细胞表面磷脂酰丝氨酸(PS)表达为对照组的2.4倍，且与红细胞粘附性相关(P=0.001)。在静态条件下，针对PS受体和Annexin V的特异性抗体可抑制RBC的黏附。在流动条件下，对CRVO红细胞的抑制作用与抗体相当，而对Annexin V的抑制作用则高出2倍。结论：CRVO红细胞黏附增加是由PS红细胞和内皮PS受体介导的。这一现象可能是CRVO发生的原因之一。
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 x 10(2) mm(-2)) compared with RAO RBC (63 +/- 5 x 10(2) mm(-2)) (P < 0.01) and normal control RBC (37 +/- 3 x 10(2) 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.