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首页> 外文期刊>The Journal of Nutritional Biochemistry >Copper promotion of angiogenesis in isolated rat aortic ring: role of vascular endothelial growth factor.
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Copper promotion of angiogenesis in isolated rat aortic ring: role of vascular endothelial growth factor.

机译：铜促进离体大鼠主动脉环中血管生成的作用：血管内皮生长因子的作用。

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摘要

Copper stimulation of angiogenesis at the organ system level is vascular endothelial growth factor (VEGF) dependent, but copper stimulation of vascular endothelial cell proliferation in cultures is VEGF independent. The present study was undertaken to use isolated rat aortic rings to understand the seemly controversial observations between in vivo and in vitro studies. The thoracic aorta was isolated from Sprague Dawley rats (8-10 weeks) and sectioned into 1.0-mm thick vascular rings for culturing. Copper sulfide at a final concentration of 5, 25, 50 or 100 micro M was added to the cultures and maintained for 8 days. A copper chelator, tetraethylenepentamine (TEPA) at a final concentration of 25 micro M, was added to some cultures to block the effect of copper. An anti-VEGF antibody was used to determine the role of VEGF in copper promotion of angiogenesis. The data obtained showed that copper at 5 micro M in cultures stimulated the vascular formation; an effect was blocked by TEPA. Copper at concentrations above 50 micro M lost the proangiogenesis effect. However, copper at 5 micro M did not enhance the production of VEGF, and concentrations above 50 micro M significantly increased VEGF production. On the other hand, the treatment with anti-VEGF antibody completely blocked the proangiogenesis effect of 5- micro M copper. This study thus demonstrates that VEGF is essential for angiogenesis but the proangiogenesis effect of copper does not act through enhanced production of VEGF.
机译：铜刺激在器官系统水平上的血管生成是依赖血管内皮生长因子（VEGF）的，但是铜刺激对培养物中血管内皮细胞增殖的依赖性是VEGF无关的。本研究的目的是使用离体的大鼠主动脉环了解体内和体外研究之间似乎有争议的观察结果。从Sprague Dawley大鼠中分离胸主动脉（8-10周），然后切成1.0毫米厚的血管环进行培养。将终浓度为5、25、50或100 micro M的硫化铜添加到培养物中，并保持8天。将最终浓度为25 micro M的铜螯合剂四亚乙基五胺（TEPA）添加到某些培养物中以阻断铜的作用。使用抗VEGF抗体来确定VEGF在铜促进血管生成中的作用。获得的数据表明，培养物中5 micro M的铜刺激了血管的形成。 TEPA阻止了这种作用。浓度高于50 micro M的铜失去了促血管生成作用。但是，铜在5 micro M时不能增强VEGF的产生，而浓度高于50 micro M则可以显着增加VEGF的产生。另一方面，抗VEGF抗体的治疗完全阻断了5-micro M铜的促血管生成作用。因此，该研究表明VEGF对于血管生成是必不可少的，但是铜的血管生成作用并不通过增强VEGF的产生而起作用。

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