Chemotaxis of aortic endothelial cells in response to fibronectin.
Chemotaxis of aortic endothelial cells in response to fibronectin.
复制标题
主动脉内皮细胞响应纤连蛋白的趋化性。
作者：
J. Bowersox;N. Sorgente
我们用盲井趋化小室测定了牛主动脉内皮细胞对纤维连接蛋白和内皮细胞有丝分裂原(内皮细胞生长补充剂、肿瘤提取物)的趋化反应。纤维连接蛋白诱导牛主动脉内皮细胞的趋化反应，在100微克/毫升时，趋化性比阴性对照组增加440%(P<0.001)。趋化反应随时间而平稳，与小室内纤维连接蛋白浓度梯度的消失平行。作为测定趋化作用的进一步证据，我们观察到，在没有浓度梯度的情况下，当细胞与纤维连接蛋白孵育时，细胞没有发生迁移。在我们的实验中，内皮细胞有丝分裂原促进了牛主动脉内皮细胞的增殖，但不能刺激高于本底水平的趋化作用。相比之下，纤维连接蛋白抑制了23%的细胞增殖。我们提出了一个假想的模型，说明在肿瘤新生血管形成过程中，纤维连接蛋白在激发内皮细胞趋化中的作用。
We have determined the chemotactic response of bovine aortic endothelial cells to fibronectin and to endothelial cell mitogens (endothelial cell growth supplement, tumor extract), using blind-well chemotaxis chambers. Fibronectin induced a chemotactic response in bovine aortic endothelial cells; at 100 micrograms/ml, chemotaxis increased by 440% above that observed in negative controls (p less than 0.001). The chemotactic response plateaued with time, paralleling the disappearance of the fibronectin concentration gradient in the chambers. As further evidence that chemotaxis was measured, we observed that cell migration did not occur when cells were incubated with fibronectin in the absence of a concentration gradient. Endothelial cell mitogens increased bovine aortic endothelial cell proliferation in our experiments but did not stimulate chemotaxis above background levels. In contrast, fibronectin inhibited cell proliferation by 23%. We present a hypothetical model of the role of fibronectin in evoking endothelial cell chemotaxis during tumor neovascularization.