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首页> 外文期刊>Journal of Cellular Physiology >Facilitated diffusion of VEGF165 through descemet's membrane with sucrose octasulfate
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Facilitated diffusion of VEGF165 through descemet's membrane with sucrose octasulfate

机译：易化扩散的VEGF165通过与蔗糖octasulfate角膜后弹力层

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Vascular endothelial growth factor A (VEGF-A) is a promoter of neovascularization and thus a popular therapeutic target for diseases involving excessive growth of blood vessels. In this study, we explored the potential of the disaccharide sucrose octasulfate (SOS) to alter VEGF165 diffusion through Descemet's membrane. Descemet's membranes were isolated from bovine eyes and used as a barrier between two chambers of a diffusion apparatus to measure VEGF transport. Diffusion studies revealed a dramatic increase in VEGF165 transport in the presence of SOS, with little diffusion of VEGF165 across the membrane over a 10-h time course in the absence of SOS. Diffusion studies with VEGF121, a non-heparin binding variant of VEGF, showed robust diffusion with or without SOS. To determine a possible mechanism, we measured the ability of SOS to inhibit VEGF interactions with extracellular matrix (ECM), using cell-free and cell surface binding assays. Binding studies showed SOS had no effect on VEGF165 binding to either heparin-coated plates or endothelial cell surfaces at less than mg/ml concentrations. In contrast, we show that SOS inhibited VEGF165 binding to fibronectin in a dose dependent manner and dramatically accelerated the rate of release of VEGF165 from fibronectin. SOS also inhibited the binding of VEGF165 to fibronectin-rich ECM deposited by vascular smooth muscle cells. These results suggest that fibronectin-rich extracellular matrices serve as barriers to VEGF165 diffusion by providing a network of binding sites that can trap and sequester the protein. Since the content of Descemet's membrane is typical of many basement membranes it is possible that they serve throughout the body as formidable barriers to VEGF165 diffusion and tightly regulate its bioavailability and distribution within tissues.
机译：血管内皮生长因子A (VEGF-A)促进新血管形成,因此很受欢迎治疗疾病涉及的目标血管的过度增长。我们探讨了潜在的二糖蔗糖octasulfate (SOS)改变VEGF165通过角膜后弹力层扩散。膜分离从牛的眼睛和使用作为扩散两院之间的一个障碍仪器测量VEGF运输。研究显示在VEGF165大幅增加运输的SOS,很少扩散的VEGF165膜上10 h时间在SOS的缺失。研究与VEGF121 non-heparin绑定VEGF的变种,或显示强劲的扩散没有紧急求救信号。我们测量SOS抑制VEGF的能力与细胞外基质(ECM)的相互作用,颗粒和细胞表面绑定化验的使用。绑定的研究显示SOS没有影响VEGF165绑定,要么heparin-coated盘子或内皮细胞表面以低于毫克/毫升浓度。纤连蛋白在抑制VEGF165绑定剂量依赖的方式和显著加速VEGF165的释放速率纤连蛋白。VEGF165 fibronectin-rich ECM沉积血管平滑肌细胞。表明fibronectin-rich细胞外矩阵作为VEGF165扩散壁垒通过提供一个网络的结合位点陷阱和隔离的蛋白质。角膜后弹力层是典型的多基底膜是可能的,他们服务整个身体强大的壁垒VEGF165扩散和其进行严格的检查生物利用度和分布在组织内。

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