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首页> 外文期刊>Journal of Cellular Physiology >Blockade of sphingosine-1-phosphate reduces macrophage influx and retinal and choroidal neovascularization.
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Blockade of sphingosine-1-phosphate reduces macrophage influx and retinal and choroidal neovascularization.

机译：封锁sphingosine-1-phosphate减少巨噬细胞和视网膜和脉络膜的涌入新生血管形成。

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摘要

Sphingosine-1-phosphate (S1P) is a bioactive lipid molecule that stimulates endothelial cell migration, proliferation, and survival in vitro, and tumor angiogenesis in vivo. In this study, we used a humanized monoclonal antibody (sonepcizumab) that selectively binds S1P to investigate its role in retinal and choroidal neovascularization (NV). Intraocular injection of sonepcizumab significantly reduced macrophage influx into ischemic retina and strongly suppressed retinal NV in mice with oxygen-induced ischemic retinopathy. In mice with laser-induced rupture sites in Bruch's membrane, intraocular injection of sonepcizumab significantly reduced the area of choroidal NV and concomitantly reduced fluorescein leakage from the remaining choroidal NV. Four weeks after intraocular injection of up to 1.8 mg of the sonepcizumab in non-human primates, electroretinograms and fluorescein angiograms were normal, and light microscopy of ocular sections showed no evidence of structural damage. These data show for the first time that S1P stimulates both choroidal and retinal NV and suggest that sonepcizumab could be considered for evaluation in patients with choroidal or retinal NV.
机译：Sphingosine-1-phosphate (S1P)是一种生物活性脂质分子刺激内皮细胞迁移、增殖和生存在体外,和体内肿瘤血管生成。用人性化单克隆抗体选择性地结合S1P (sonepcizumab)探讨它在视网膜和脉络膜的角色新血管形成(NV)。sonepcizumab显著降低巨噬细胞流入到缺血性视网膜和强烈抑制视网膜NV与oxygen-induced老鼠缺血性视网膜病变。网站在布鲁赫膜破裂,眼内注入sonepcizumab明显减少了脉络膜的NV的面积,与此同时从剩余的降低荧光素渗漏脉络膜的NV, 4周后眼内注入的sonepcizumab 1.8毫克非人类的灵长类动物,网膜电图荧光素血管造影检查是正常的,光显微镜的目镜部分显示没有证据结构性破坏。第一次S1P刺激和脉络膜的视网膜NV,表明sonepcizumab考虑患者的评估脉络膜和视网膜NV。

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