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）是免疫应答、造血和急性期反应的多功能调节因子，被认为对肿瘤细胞有直接和/或间接的作用。近年来，有研究表明，血清白细胞介素-6（IL-6）水平和癌组织中IL-6的表达与各种癌症患者的预后相关。本研究探讨了IL-6和G-CSF对内皮细胞增殖和血管生成的影响。使用内皮细胞系HUV-EC-C（人，血管内皮，脐静脉）和MS 1VEGF（小鼠，胰腺静脉，SV 40转化的;用VEGF载体感染）。IL-6和G-CSF不促进HUV-EC-C和MS 1 VEGF的增殖。血管生成试验：该血管生成试验代表了一种血管生成模型，其中IL-6和G-CSF诱导的血管生成是由VEGF诱导的。 ...更多信息 r抑制管形成。试验说明;一曰：使用Labtec II腔室载玻片，2：将200μL纤维蛋白原溶液分配到腔室载玻片中，3：向腔室中加入13312 L/孔凝血酶，4：将载玻片在37℃下放置60 min以进行孵育，5：将HUV-EC-C和MS 1 VEGF以5 × 10^4细胞-mL的终浓度重悬于培养基中，6：在小室玻片的孔中加入1000 μL HUV-EC-C和MS 1 VEGF，7：在小室玻片的孔中加入200μL纤维蛋白原，8：在小室玻片的孔中加入133 μL凝血酶，8：置于37℃ 5%CO_2培养箱中。血管生成实验中，HUV EV-C可观察到血管生成，而产生高VEGF的MS 1 VEGF在血管生成实验中未观察到血管生成。bFGF 50μg/ml和/或PMA 50μg/ml可促进HUV-EC-C的血管生成。另外，bFGF 50μg/ml和/或PMA 50μg/ml对MS 1 VEGF的血管生成无促进作用。MS 1 VEGF产生高VEGF，具有高的增殖潜力，但MS 1 VEGF显示较差的血管生成（毛细血管形成）。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导致肿瘤组织中血管未成熟。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