Nitric oxide is proangiogenic in the retina and choroid
Nitric oxide is proangiogenic in the retina and choroid
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DOI：
10.1002/jcp.10083
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发表时间：
2002-04-01
影响因子：
5.6
通讯作者：
Campochiaro, PA
中科院分区：
文献类型：
--
作者：
Ando, A;Yang, A;Campochiaro, PA
一氧化氮（NO）已显示出具有促血管生成或抗血管生成作用，这取决于环境。在这项研究中，我们使用的小鼠有针对性地删除一氧化氮合酶（NOS）的三种亚型之一，以探讨NO在眼部新生血管的影响。在转基因小鼠的血管内皮生长因子（VEGF）的表达增加的光感受器，缺乏任何三种亚型引起视网膜下新生血管的显着减少，但没有改变VEGF的表达。在激光诱导Bruch膜破裂的小鼠中，诱导型NOS（iNOS）或神经元型NOS（nNOS）的缺乏，而不是内皮型NOS（eNOS），导致脉络膜新生血管的显着减少。在氧诱导的缺血性视网膜病变小鼠中，eNOS缺乏而不是iNOS或nNOS缺乏导致视网膜新生血管显著减少和VEGF表达减少。这些数据表明，NO有助于视网膜和脉络膜新生血管和NOS的不同亚型参与不同的设置和不同的疾病过程。广谱NOS抑制剂可能具有治疗视网膜和脉络膜新生血管的治疗潜力。J.细胞。191：116-124，2002。(C)2002 Wiley-Liss，Inc.
itric oxide (NO) has been shown to have proangiogenic or antiangiogenic effects depending upon the setting. In this study, we used mice with targeted deletion of one of the three isoforms of nitric oxide synthase (NOS) to investigate the effects of NO in ocular neovascularization. In transgenic mice with increased expression of vascular endothelial growth factor (VEGF) in photoreceptors, deficiency of any of the three isoforms caused a significant decrease in subretinal neovascularization, but no alteration of VEGF expression. In mice with laser-induced rupture of Bruch's membrane, deficiency of inducible NOS (iNOS) or neuronal NOS (nNOS), but not endothelial NOS (eNOS), caused a significant decrease in choroidal neovascularization. In mice with oxygen-induced ischemic retinopathy, deficiency of eNOS, but not iNOS or nNOS caused a significant decrease in retinal neovascularization and decreased expression of VEGF. These data suggest that NO contributes to both retinal and choroidal neovascularization and that different isoforms of NOS are involved in different settings and different disease processes. A broad spectrum NOS inhibitor may have therapeutic potential for treatment of both retinal and choroidal neovascularization. J. Cell. Physiol. 191: 116-124, 2002. (C) 2002 Wiley-Liss, Inc.