INDUCTION OF HUMAN VASCULAR ENDOTHELIAL STRESS FIBERS BY FLUID SHEAR-STRESS
INDUCTION OF HUMAN VASCULAR ENDOTHELIAL STRESS FIBERS BY FLUID SHEAR-STRESS
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DOI：
10.1038/307648a0
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发表时间：
1984-01-01
期刊：
影响因子：
64.8
通讯作者：
DRENCKHAHN, D
中科院分区：
文献类型：
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作者：
FRANKE, RP;GRAFE, M;DRENCKHAHN, D
动脉血管系统和心脏的内皮细胞含有直的肌动蛋白细丝束，在静脉内皮中即使有也很少。由于血管系统中含有应力纤维的内皮细胞往往位于暴露于血流剪切应力特别高的部位，因此我们在实验流变系统中（图1）研究了内皮肌动蛋白丝骨架对受控流体剪切应力水平的反应。在这里，我们报告了内皮应力纤维可以通过将人血管内皮的融合单层培养物暴露于2 dynes cm - 2的流体剪切应力3小时来诱导，近似于人动脉在体内发生的应力。正常情况下仅发生在静脉中的四倍剪切应力对内皮肌动蛋白丝系统没有显著影响。内皮应力纤维的形成响应临界水平的流体剪切应力可能是一个功能上重要的机制，保护内皮免受水动力损伤和脱离。
Endothelial cells of the arterial vascular system and the heart contain straight actin filament bundles, of which there are few, if any, in the venous endothelium1–4. Since stress fibre-containing endothelial cells within the vascular system tend to be located at sites exposed to particularly high shear stress of blood flow, we have investigated, in an experimental rheological system (Fig. 1), the response of the endothelial actin filament skeleton to controlled levels of fluid shear stress. Here we report that endothelial stress fibres can be induced by a 3-h exposure of confluent monolayer cultures of human vascular endothelium to a fluid shear stress of 2 dynes cm−2, approximately the stress occurring in human arteriesin vivo. Fourfold lower levels of shear stress that normally occur only in veins, had no significant effect on the endothelial actin filament system. The formation of endothelial stress fibres in response to critical levels of fluid shear stress is probably a functionally important mechanism that protects the endothelium from hydrodynamic injury and detachment.