...
首页> 外文期刊>Critical Reviews in Biomedical Engineering >Mechanics of endothelial cell architecture and vascular permeability [Review]
【24h】

Mechanics of endothelial cell architecture and vascular permeability [Review]

机译:内皮细胞结构和血管通透性的机制[综述]

获取原文
获取原文并翻译 | 示例
           

摘要

Blood vessel walls form a selective barrier to the transport of materials between blood and tissue, and the endothelium contributes significantly to this barrier function. The role of the endothelium is particularly important in thin-walled vessels, such as venules, because during tissue inflammation the endothelial junctions widen in localized areas and gaps form, thus compromising the barrier function. The mechanisms of endothelial gap formation are still under question. In this review we describe what is known about the structure of endothelial cell-cell junctions and how this structure can change during inflammation. We then consider two possible mechanisms by which endothelial gaps are formed: active endothelial cell contraction or breakdown of the junctional complex, followed by passive recoil. Using measured values of the mechanical properties of endothelial cells, and the forces to which they are subjected, we calculate that gap formation by breakdown of cellular adhesion, followed by passive recoil, is a feasible mechanism. Finally, since endothelial cell surfaces, including junctions, are coated with a glycocalyx, we consider the question of whether changes in the glycocalyx can markedly increase endothelial permeability. We conclude that gap formation can occur by active contraction or by breakdown of adhesion, depending on the inflammatory mediator, and that the responses of the glycocalyx may also play an important role in the regulation of microvascular permeability. [References: 123]
机译:血管壁形成了对材料在血液和组织之间运输的选择性屏障,并且内皮显着地促进了这种屏障功能。内皮的作用在薄壁血管(如小静脉)中尤其重要,因为在组织发炎期间,内皮连接在局部区域和间隙处变宽,从而损害了屏障功能。内皮间隙形成的机制仍存在疑问。在这篇综述中,我们描述了有关内皮细胞-细胞连接结构的知识,以及该结构在炎症过程中如何变化。然后,我们考虑形成内皮间隙的两种可能的机制:主动内皮细胞收缩或连接复合体破裂,然后被动后坐。使用内皮细胞的机械性能的测量值以及它们所承受的力,我们计算出通过细胞粘附力的破坏形成间隙,然后进行被动反冲,是一种可行的机制。最后,由于内皮细胞表面(包括连接处)都涂有糖萼,因此我们考虑糖萼的变化是否能显着增加内皮通透性的问题。我们得出的结论是,间隙形成可以通过主动收缩或粘附破坏而发生,具体取决于炎性介质,并且糖萼的反应也可能在微血管通透性的调节中起重要作用。 [参考:123]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号