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Involvement of Vascular Endothelial Growth Factor in Kaposis Sarcoma Associated with Acquired Immunodeficiency Syndrome

机译:血管内皮生长因子参与后天性免疫缺陷综合症的卡波济肉瘤

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摘要

To examine the role of vascular endothelial growth factor (VEGF) in the development of edema associated with Kaposi's sarcoma (KS) in acquired immunodeficiency syndrome (AIDS), we exploited animal model systems to detect the activity that induces vascular hyper‐permeability (VHP) using cultured AIDS‐KS spindle cells. Cultured AIDS‐KS spindle cells and conditioned medium (AIDS‐KS‐CM) that had been semi‐purified through a heparin affinity column were tested for the ability to induce VHP in animals. The AIDS‐KS spindle cells and AIDS‐KS‐CM induced VHP that was histamine‐independent. The VHP‐inducing activity was detected in the 0.5 M NaCl fraction from the heparin affinity column and was blocked by anti‐VEGF neutralizing antibody. In addition, the production of VEGF was demonstrated in fresh AIDS‐KS tissue as well as in cultured AIDS‐KS cells, while control cells were negative for VEGF production. From these observations, we concluded that AIDS‐KS cells produce a factor(s) that promotes VHP, and this factor could be VEGF.
机译:为了检查血管内皮生长因子(VEGF)在获得性免疫缺陷综合症(AIDS)中与卡波济肉瘤(KS)相关的水肿发展中的作用,我们利用动物模型系统来检测诱导血管高通透性(VHP)的活性使用培养的AIDS‐KS梭形细胞。测试了通过肝素亲和柱半纯化的培养的AIDS-KS梭形干细胞和条件培养基(AIDS-KS-CM)诱导动物体内VHP的能力。 AIDS-KS纺锤体细胞和AIDS-KS-CM诱导的VHP独立于组胺。在肝素亲和柱的0.5 M NaCl馏分中检测到VHP诱导活性,并被抗VEGF中和抗体阻断。此外,在新鲜的AIDS-KS组织以及培养的AIDS-KS细胞中都证明了VEGF的产生,而对照细胞中VEGF的产生却是阴性的。从这些观察结果,我们得出结论,AIDS-KS细胞产生促进VHP的因子,而该因子可能是VEGF。

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