Oxidized-LDL induce morphological changes and increase stiffness of endothelial cells
Oxidized-LDL induce morphological changes and increase stiffness of endothelial cells
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DOI：
10.1016/j.yexcr.2008.07.020
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发表时间：
2008-10-01
影响因子：
3.7
通讯作者：
Vermette, Patrick
中科院分区：
文献类型：
--
作者：
Chouinard, Julie A.;Grenier, Guillaume;Vermette, Patrick
越来越多的证据表明氧化低密度脂蛋白（ox-LDL）在动脉粥样硬化的血管内皮损伤中起重要作用。在这项研究中，天然LDL和氧化型LDL对活的人脐静脉内皮细胞（HUVEC）的力学性能的影响进行了研究，通过原子力显微镜（AFM）的力测量。用荧光显微镜观察了丝状肌动蛋白（F-actin）和波形蛋白对细胞骨架网络结构的影响。我们的研究结果表明，ox-LDL通过干扰F-actin和vimentin对HUVEC的形状产生影响，而天然LDL则没有影响。AFM胶体力测量活个体HUVEC上成功地用于测量暴露于天然和ox-LDL的细胞的刚度。AFM结果表明，当细胞暴露于ox-LDL 24 h时，细胞体变得明显僵硬，而暴露于天然LDL 24 h的细胞显示出与对照细胞相似的刚度。使用两种模型计算LDL暴露的HUVEC的杨氏模量。因此，这项研究提供了定量证据的生物力学机制相关的内皮细胞功能障碍，并可能提供新的见解的战略，旨在保护内皮功能在动脉粥样硬化。(C)2008年爱思唯尔公司All rights reserved.
There is increasing evidence suggesting that oxidized low-density lipoproteins (ox-LDL) play a Critical role in endothelial injury contributing to the age-related physio-pathological process of atherosclerosis. In this Study, the effects of native LDL and ox-LDL on the mechanical properties of living human umbilical vein endothelial cells (HUVEC) were investigated by atomic force microscopy (AFM) force measurements. The contribution of filamentous actin (F-actin) and vimentin on cytoskeletal network Organization were also examined by fluorescence microscopy. Our results revealed that ox-LDL had an impact on the HUVEC shape by interfering with F-actin and vimentin while native LDL showed no effect. AFM colloidal force measurements on living individual HUVEC were successfully used to measure stiffness of cells exposed to native and ox-LDL. AFM results demonstrated that the cell body became significantly stiffer when cells were exposed for 24 h to ox-LDL while cells exposed for 24 h to native LDL displayed similar rigidity to that of the control cells. Young's moduli of LDL-exposed HUVEC were calculated using two models. This study thus provides quantitative evidence on biomechanical mechanisms related to endothelial cell dysfunction and may give new insight on strategies aiming to protect endothelial function in atherosclerosis. (C) 2008 Elsevier Inc. All rights reserved.