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

白细胞介素6(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，对肿瘤细胞具有直接和/或间接作用。近年来，有报道称血清白介素6(IL-6)水平和癌组织中IL-6的表达与多种癌症患者的预后有关。在本研究中，我们观察了IL-6或G-CSF对血管内皮细胞增殖和血管生成能力的影响。使用血管内皮细胞系HuV-EC-C(人，血管内皮细胞，脐静脉)和MS1 VEGF(小鼠，胰腺静脉，SV40转化；感染血管内皮生长因子载体)。IL-6和G-csf对HUV-EC-C和MS1-…的增殖无明显促进作用。血管生成实验：该血管生成实验代表了一种血管生成的模型对管子形成的抑制作用更强。化验说明；1：采用Labtec II载玻片，2：向载玻片中加入200μ的L纤维蛋白原溶液，3：向载玻片中加入13312℃的L纤维蛋白原，4：将载玻片置于37℃下60min进行聚合，5：将hUV-EC-C和MS1血管内皮生长因子以最终浓度5×10~(-4)细胞/毫升悬浮于载玻片中，6：在载玻片中加入1000个/μ的L hIV-EC-C和MS1血管内皮生长因子，7：向载玻片中加入200μ的L纤维蛋白原，8：在载玻片中加入133μL，血管生成：HUVEV-C在血管生成实验中观察到血管生成，而Ms1-℃在血管生成实验中未观察到血管生成。BFGF50μg/ml和/或PMA50μg/m可促进血管生成，而bFGF50μg/ml和/或PMA50μg/m不能促进血管生成。高表达血管内皮生长因子的MS1细胞具有较高的增殖潜能，但其血管生成能力较差(毛细血管形成)。血管内皮生长因子可促进内皮细胞的增殖，但不能促进血管生成(毛细血管形成)。因此，血管内皮生长因子导致了肿瘤组织中未成熟的血管。较少

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