Suramin inhibits C6 glioma‐induced angiogenesis in vitro
Suramin inhibits C6 glioma‐induced angiogenesis in vitro
复制标题
苏拉明体外抑制 C6 胶质瘤诱导的血管生成
DOI：
--
复制
发表时间：
1995
影响因子：
4
通讯作者：
B. Coomber
中科院分区：
文献类型：
--
作者：
B. Coomber
在C6细胞（一种实验衍生的大鼠神经胶质肿瘤细胞系）产生的无血清条件培养基的影响下，利用牛内皮细胞表面单层的胶原凝胶入侵实验，研究了肿瘤诱导的体外血管生成的各个方面。我们对已知干扰生长因子/细胞信号的多阴离子化合物苏拉明在这一过程中的作用进行了评估。在transwell插入物中，将含有或不含不同剂量苏拉明的C6条件培养基添加到在I型胶原凝胶上生长的牛主动脉内皮细胞的单层中，定量测定胶原凝胶的侵袭。用相差显微镜监测培养物。经过不同时期的孵育，将胶原凝胶固定，包埋在环氧树脂中，并用甲苯胺蓝染色1 μm厚的切片。另外用C6条件培养基和苏拉明对内皮细胞增殖的影响，以及通过8 μm孔的趋化性。C6胶质瘤细胞条件培养基诱导大血管内皮细胞向胶原基质中生长，随后从毛细血管样管网络中生长。条件培养基对这些细胞也具有趋化和有丝分裂作用。在C6胶质瘤条件培养基中添加苏拉明可阻止胶原凝胶中的管状形成，并以剂量依赖性的方式抑制内皮细胞增殖和趋化。这些结果表明，胶质肿瘤细胞条件培养基通过被苏拉明破坏的机制诱导体外大血管内皮细胞的血管生成，最有可能涉及肿瘤来源的生长因子释放和/或内皮介导的基质蛋白水解。
Aspects of tumor‐induced angiogenesis in vitro were examined using an assay involving collagen gel invasion by a surface monolayer of bovine endothelial cells under the influence of serum free conditioned medium produced by C6 cells, an experimentally derived rat glial tumor cell line. The effects of the polyanionic compound suramin, known to interfere with growth factor/cell signaling on this process were evaluated. Collagen gel invasion was quantified by adding C6 conditioned medium with or without various doses of suramin to monolayers of bovine aortic endothelial cells grown on type I collagen gels in transwell inserts. Cultures were monitored with phase‐contrast microscopy. After various periods of incubation collagen gels were fixed, embedded in epoxy resin, and 1‐μm thick sections were stained with toluidine blue. Additional cultures were used to evaluate the effects of C6 conditioned medium and suramin on endothelial cell proliferation, and on chemotaxis through 8‐μm pores. C6 glioma cell conditioned medium induced large vessel endothelial cells to sprout into the underlying collagen matrix and subsequently from networks of capillary like tubes. Conditioned medium was also chemotactic and mitogenic for these cells. The addition of suramin to C6 glioma conditioned medium prevents tube formation in collagen gels, and inhibits both endothelial cell proliferation and chemotaxis in a dose dependent manner. These results suggest that glial tumor cell conditioned medium induces angiongenesis in large vessel endothelial cells in vitro via mechanisms which are disrupted by suramin, most likely involving tumor‐derived growth factor release and/or endothelium‐mediated matrix proteolysis.
登录
查看更多内容
DOI：
--
发表时间：
1992-05
期刊：
Laboratory investigation; a journal of technical methods and pathology
影响因子：
--
作者：
R. Vernon;J. Angello;M. Iruela-Arispe;T. Lane;E. Sage
通讯作者：
R. Vernon;J. Angello;M. Iruela-Arispe;T. Lane;E. Sage
HGF-SF 与其他细胞因子在肿瘤侵袭和血管生成中的相互作用。
DOI：
--
发表时间：
1993
期刊：
EXS
影响因子：
--
作者：
Rosen,EM;Zitnik,RJ;Elias,JA;Bhargava,MM;Wines,J;Goldberg,ID
通讯作者：
Goldberg,ID
通过表达反义胰岛素样生长因子 I RNA 的免疫原性 C6 细胞治疗和预防大鼠胶质母细胞瘤。
DOI：
10.1126/science.8418502
发表时间：
1993
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Trojan,J;Johnson,TR;Rudin,SD;Ilan,J;Tykocinski,ML;Ilan,J
通讯作者：
Ilan,J
影响因子：
3.3
作者：
GOLDMAN, CK;KIM, J;GILLESPIE, GY
通讯作者：
GILLESPIE, GY
影响因子：
11.2
作者：
Anthony;M. P. Montgomery;Y. Clerck;Keith E. Langley;Ralph A. Reisfeld;Barbara;M. Mueller
通讯作者：
Anthony;M. P. Montgomery;Y. Clerck;Keith E. Langley;Ralph A. Reisfeld;Barbara;M. Mueller