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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Low-density lipoprotein induced actin cytoskeleton reorganization in endothelial cells: mechanisms of action.
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Low-density lipoprotein induced actin cytoskeleton reorganization in endothelial cells: mechanisms of action.

机译：低密度脂蛋白诱导内皮细胞肌动蛋白细胞骨架重组：作用机理。

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摘要

The inhibitory effects of the specific NADPH oxidase inhibitor, apocynin, and non-specific NADPH oxidase inhibitors, nordihydroguaiaretic acid (NDGA) and SKF525A, on the disruption of dense peripheral bands and formation of stress fibers in cultured human umbilical vein endothelial cells exposed to atherogenic low-density lipoprotein (LDL) levels has been investigated. Endothelial cells (EC) in vitro and in vivo exposed to high LDL-cholesterol levels have cytoskeletal remodeling with stress fiber formation and loss of dense peripheral bands. Cultured EC incubated with exogenously applied hydrogen peroxide (H2O2: 1 mM) have cytoskeletal structural changes much similar to those observed with high LDL exposure. Previous studies have 1) demonstrated that exposure to atherogenic LDL levels causes heightened EC H2O2 production, 2) identified the reactive oxygen species source, NADPH oxidase, in EC, and 3) shown that the specific NADPH oxidase inhibitor, apocynin, and non-specific NADPH oxidase inhibitors, NDGA and SKF525A, suppress H2O2 production increases in high LDL-perturbed EC. In the present study, the cytoskeletal structure of EC exposed to 330 mg/dl LDL-cholesterol, and incubated with or without apocynin, NDGA and SKF525A, was examined. Each of these compounds promoted the retention of dense peripheral bands and minimized stress fiber formation. These findings are consistent with NADPH oxidase and it's reactive oxygen species byproducts modulating the cytoskeleton reorganization observed in high LDL-induced EC perturbation.
机译：特定的NADPH氧化酶抑制剂，载脂蛋白和非特定的NADPH氧化酶抑制剂，去氢二氢愈创木酸（NDGA）和SKF525A对暴露于致动脉粥样硬化的人脐静脉内皮细胞中致密的外周带破坏和应力纤维形成的抑制作用低密度脂蛋白（LDL）水平已得到研究。体外和体内暴露于高LDL-胆固醇水平的内皮细胞（EC）具有重塑应力纤维并失去密集的外周带的细胞骨架重塑。与外源施加的过氧化氢（H2O2：1 mM）一起孵育的培养EC具有与高LDL暴露下观察到的细胞骨架结构变化非常相似的结构。先前的研究已经证明1）暴露于致动脉粥样硬化的低密度脂蛋白水平会导致EC H2O2的产生增加; 2）确定了EC中的活性氧源NADPH氧化酶，以及3）表明特定的NADPH氧化酶抑制剂，载脂蛋白和非特异性NADPH氧化酶抑制剂NDGA和SKF525A抑制高LDL干扰的EC中H2O2产量的增加。在本研究中，检查了暴露于330 mg / dl LDL-胆固醇并与或不与Apocynin，NDGA和SKF525A一起孵育的EC的细胞骨架结构。这些化合物中的每一种都促进了致密外围带的保留并最大程度地减少了应力纤维的形成。这些发现与NADPH氧化酶和其活性氧副产物调节在高LDL诱导的EC扰动中观察到的细胞骨架重组一致。

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