中文摘要：

背景 Choroidal neovascularization (CNV ) 是在有年龄相关的有斑点的退化的老病人的视觉损失的一个普通原因并且代表 subretinal 的生长在有斑点的区域的新容器。这研究试图在氩激光的一个老鼠模型在 CNV.Methods 调查在 annexin A2 ( ANXA2 )和脉管的 endothelial 生长因素( VEGF )之间的关系导致凝结的 CNV ， annexins 的 mRNA 表情和在视网膜的 VEGF 蛋白质表示被检测用荧光灯即时聚合酶链反应( PCR )和 immunohistochemistry 分别地。在在两个的 ANXA2 和 VEGF 之间的相互作用上皮的房间线 RPE-J 和老鼠 CNV 建模的网膜的颜料借助于 RNA 干扰，即时 PCR，西方的弄污的、连接酶的 immunosorbent 试金(ELISA ) 和组织病理学说的考试被检验。结果宫底荧光黄 angiography (船边交货) 证明视网膜的氩激光凝结在老鼠劝诱了稳定的 CNV 模特儿。在凝结以后的二～三个星期， ANXA2。并且当另外的 annexin 成员(ANXA4， ANXA5， ANXA7 和 ANXA11 ) 没显示出明显的变化时，在在视网膜和脉络膜的凝结的区域的 VEGF 表情增加了到山峰水平。在 RPE-J 房间和 CNV 模型， ANXA2 基因的 RNA 干扰显著地降低了在老鼠的增加的 VEGF 表达式 CNV 建模的显著地包含 ANXA2 基因的 adenoviral 向量的 VEGF 蛋白质和 mRNA 表达式，和应用程序，但是没在 kinase 的表达式上生产重要效果插入包含域的受体( KDR )或象fms一样酷氨酸 kinase ( Fit-l )。KDR 的表示在 ANXA2 表示，而是 VEGF 和 Rt-1 禁止了增长直接没影响 ANXA2 表示。除是的角色以外的结论 plasminogen 和织物 plasminogen 使活跃之物的受体， ANXA2，在经由否定反馈机制的 KDR 的规定下面，也由通过积极反馈机制调整 VEGF 表示参予 neovascularization。

英文摘要：

Background Choroidal neovascularization （CNV） is a common cause of visual loss in the elderly patients with age-related macular degeneration and represents the growth of subretinal new vessels in the macular region. This study aimed to investigate the relationship between annexin A2 （ANXA2） and vascular endothelial growth factor （VEGF） in CNV.Methods In a rat model of argon laser coagulation-induced CNV, the mRNA expressions of the annexins and VEGF protein expression in the retina were detected using fluorescent real-time polymerase chain reaction （PCR） and immunohistochemistry, respectively. The interactions between ANXA2 and VEGF in both a retinal pigment epithelial cell line RPE-J and the rat model of CNV were examined by means of RNA interference, real-time PCR, Western blotting, enzyme-linked immunosorbent assay （ELISA） and histopathological examinations. Results Fundus fluorescein angiography （FFA） showed that argon laser coagulation of the retina induced stable CNV models in the rats. Two to three weeks after the coagulation, ANXA2. and VEGF expressions in the coagulated area in the retina and choroid increased to the peak level, while the other annexin members （ANXA4, ANXA5, ANXA7 and ANXA11） showed no obvious changes. In RPE-J cells and the CNV model, RNA interference of ANXA2 gene significantly lowered the VEGF protein and mRNA expressions, and application of an adenoviral vector containing ANXA2 gene markedly increased VEGF expressions in the rat model of CNV, but produced no significant effects on the expressions of the kinase insert domain-containing receptor （KDR） or the fms-like tyrosine kinase （Fit-l）. The expression of KDR inhibited the increment in ANXA2 expression, but VEGF and Rt-1 did not directly affect ANXA2 expression. Conclusion Besides the role as a plasminogen and the receptor of tissue plasminogen activator, ANXA2, which is under regulation of KDR via a negative feedback mechanism, also participates in neovascularization by regulating VEGF expressio