Angiogenesis Induced by IL-6 and G-CSF in Rumor Tissue

白细胞介素(IL)-6和粒细胞刺激因子（G-CSF）是免疫反应、造血和急性期反应的多功能调节剂，可能对癌细胞有直接和/或间接的作用。近年来，有报道称血清白细胞介素-6 （IL-6）水平及癌组织表达与多种癌症患者的预后相关。在本研究中，我们研究了IL-6或G-CSF对内皮细胞增殖和血管生成潜能的影响。使用内皮细胞系HUV-EC-C（人，血管内皮，脐静脉）和MS1 VEGF（小鼠，胰腺静脉，SV40转化；感染VEGF载体）。增殖：MS1 VEGF的增殖潜力明显高于HUV-EC-C。IL-6和G-CSF对HUV-EC-C和MS1 VEGF的增殖无促进作用。血管生成试验：这种血管生成试验代表了一种血管生成模型，其中诱导或抑制管的形成。化验说明；1: Labtec二室的幻灯片,2:分发200μL纤维蛋白原解室的幻灯片,3:加上13312 L /凝血酶室,4:幻灯片在37℃聚合60分钟,5:HUV-EC-C和MS1 VEGF resuspend最终浓度为5×10 ^ 4萤光在媒体,6:增加1000 /μL HUV-EC-C和MS1 VEGF在室幻灯片,7:添加200μL /纤维蛋白原在室幻灯片,8:添加133μL /凝血酶在室幻灯片,8:置于37℃5%CO_2培养箱中。血管生成：HUV EV-C在血管生成实验中观察到血管生成，而产生高VEGF的MS1在血管生成实验中未观察到血管生成。bFGF 50μg/ml和PMA 50μg/m可促进HUV-EC-C的血管生成。另外，bFGF 50μg/ml和PMA 50μg/m对MS1 VEGF的血管生成没有促进作用。结论：VEGF促进内皮细胞增殖。产生高VEGF的MS1 VEGF具有较高的增殖潜能，但MS1 VEGF血管生成（毛细血管形成）较差。VEGF促进内皮细胞增殖，但不促进血管生成（毛细血管形成）。因此VEGF导致肿瘤组织中的未成熟血管。少

Interleukin (IL)-6 and granulocyte-stimulating factor (G-CSF) are multifunctional regulator of immune response, hematopoiesis and acute phase reaction, and suppose to have the direct and/or indirect effect to the cancer cells. Recently, it has been reported that serum levels of interleukin-6 (IL-6) and expression in cancer tissues are correlated with the prognosis in various cancer patients. In this present study, we investigated that whether the proliferation and angiogenesis potential were influenced with IL-6 or G-CSF treatment in endothelial cells. Endothelial cell lines, HUV-EC-C (human, vascular endothelium, umbilical vein) and MS1 VEGF (Mouse, Pancreas vein, SV40 transformed; infected with a vector for VEGF) were used.Proliferation : MS1 VEGF was observed higher potential of proliferation than HUV-EC-C. IL-6 and G-CSF did not enhance the proliferation of HUV-EC-C and MS1 VEGF.Angiogenesis Assay : This angiogenesis assay represents a model of angiogenesis in which the induction o … More r inhibition of tube formation. Assay instructions ; 1 : Labtec II chamber slides was used, 2 : Dispense 200μL fibrinogen solution into the chamber slides, 3 : Add 13312 L per well thrombin to the chamber, 4 : Place slides at 37℃ for 60 min to polymerize, 5 : HUV-EC-C and MS1 VEGF were resuspend at a final concentration of 5 X 10^4 cells-mL in media, 6 : Add 1000 /μL HUV-EC-C and MS1 VEGF in well in chamber slides, 7 : Add 200μL per well fibrinogen in chamber slides, 8 : Add 133 μL per well thrombin in chamber slide, 8 : Place in 37℃ 5%CO_2 incubator.Angiogenesis: HUV EV-C was observed angiogenesis in angiogenesis assay, but MS1 VEGF which producted high VEGF was not observed angiogenesis in angiogenesis assay. Angiogenesis of HUV-EC-C was enhanced by bFGF 50μg/ml and/or PMA 50μg/m. Otherwise, Angiogenesis of MS1 VEGF was not enhanced by bFGF 50μg/ml and/or PMA 50μg/m.Conclusion: VEGF enhanced the proliferation of endothelial cells. MS1 VEGF which products high VEGF has high potential of proliferation, but MS1 VEGF showed poor angiogenesis (capillary formation). VEGF enhanced proliferation but not angiogenesis (capillary formation) of endothelial cells. So VEGF cause the immature vessels in tumor tissue. Less