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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Mechanotransduction of endothelial oxidative stress induced by cyclic strain.
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Mechanotransduction of endothelial oxidative stress induced by cyclic strain.

机译：循环应变诱导的内皮细胞氧化应激的机械转导。

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摘要

Atherosclerotic lesions display a nonuniform distribution throughout the vascular tree. Mechanical forces produced by local alterations in blood flow may play an important role in the localization of atherosclerosis. One such force, cyclic strain, has been hypothesized to promote atherogenesis by inducing oxidative stress in endothelial cells, resulting in enhanced endothelial adhesiveness for monocytes. To investigate the signal transduction systems involved, human aortic endothelial cells were plated on flexible silicone strips that were either non-coated or adsorbed with poly-L-lysine, vitronectin, fibronectin, or collagen I. Cells were then subjected to uniform sinusoidal stretch (10%) for 6 h. Endothelial superoxide anion production was increased in cells exposed to cyclic strain compared to static conditions. Furthermore, endothelial oxidative response to stretch was matrix protein-dependent, whereas cells grown on fibronectin and collagen I produced significantly more superoxide. The oxidative response to cyclic strain was reduced by coincubation with RGD peptides, blocking antibodies to alpha2- and beta-integrins antibodies, as well as inhibitors of protein kinase C. To investigate the effect of oxidative stress on gene transcription, endothelial cells grown on collagen I were transfected with an NFkappaB-sensitive luciferase construct. Cells that underwent cyclic strain displayed a tenfold induction of NFkappaB activation compared to static controls. Strain-induced luciferase activity was blunted by coincubation with RGD peptides or calphostin C. Thus, exposure of endothelial cells to cyclic strain led to integrin activation of a PKC-sensitive pathway that results in increased superoxide anion production and mobilization of NFkappaB.
机译：动脉粥样硬化病变在整个血管树中显示出不均匀的分布。局部血流变化产生的机械力可能在动脉粥样硬化的定位中起重要作用。已经假设一种这样的力，即循环应变，通过在内皮细胞中诱导氧化应激来促进动脉粥样硬化，从而导致单核细胞的内皮粘附性增强。为了研究涉及的信号转导系统，将人类主动脉内皮细胞铺在未涂覆或吸附有聚L-赖氨酸，玻连蛋白，纤连蛋白或胶原蛋白I的柔性硅胶条上。然后对细胞进行均匀的正弦拉伸（ 10％）持续6小时。与静态条件相比，暴露于循环应变的细胞中内皮超氧化物阴离子的产生增加。此外，内皮细胞对拉伸的氧化反应是基质蛋白依赖性的，而在纤连蛋白和胶原蛋白I上生长的细胞产生的超氧化物明显更多。通过与RGD肽共孵育，阻断针对α2和β整联蛋白的抗体以及蛋白激酶C的抑制剂，可以减少对循环菌株的氧化反应。为了研究氧化应激对基因转录的影响，胶原蛋白上生长的内皮细胞我被NFkappaB敏感的荧光素酶构建体转染。与静态对照相比，经历了循环应变的细胞显示出十倍的NFkappaB激活诱导。通过与RGD肽或钙磷蛋白C共温育，菌株诱导的荧光素酶活性减弱。因此，内皮细胞暴露于环状菌株会导致PKC敏感途径的整联蛋白活化，从而导致超氧化物阴离子产生增加和NFkappaB的动员。

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