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首页> 外文期刊>Journal of Cellular Physiology >Modulating endothelial barrier function by targeting vimentin phosphorylation
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Modulating endothelial barrier function by targeting vimentin phosphorylation

机译：调节内皮屏障功能针对波形蛋白磷酸化

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摘要

Vimentin is a major intermediate filament protein in vascular endothelial cells which might be involved in their function as a barrier tissue. It is proposed to dynamically maintain integrity of the endothelium as a tightly regulated permeability barrier that is subjected to a variety of shear and contractile forces. The results described in this report demonstrate that vimentin plays that role through mechanisms that are dependent on its phosphorylation state. Withaferin A (WFA), a vimentin targeting drug is shown to disrupt endothelial barrier function through its effects on vimentin filament distribution and physical properties. These effects are related to WFA's ability to increase vimentin phosphorylation. Through overexpressing a non-phosphorylatable vimentin mutant we can block the effects of WFA on vimentin distribution and barrier permeability. The barrier augmentation effect appears to extend to endothelial cells that do not express detectable mutant vimentin which might suggest transmissible effects across cells. Blocking vimentin phosphorylation also protects the endothelial barrier against LPS endotoxin, implicating it as a target for drug development against pulmonary edema and acute respiratory distress syndrome (ARDS).
机译：波形蛋白是主要的中间丝蛋白在血管内皮细胞组织参与他们的功能障碍。提出了动态保持完整性内皮的严格监管渗透率受到障碍各种各样的剪切和收缩力。结果本报告所描述的证明波形蛋白通过机制扮演这个角色依赖于其磷酸化状态。Withaferin (WFA)、波形蛋白靶向药物显示破坏内皮屏障功能通过对波形蛋白纤维的影响分布和物理特性。影响相关WFA增加的能力波形蛋白磷酸化。一个non-phosphorylatable波形蛋白突变体块WFA在波形蛋白分布的影响渗透率和障碍。增强效应似乎扩展内皮细胞不表达检测波形蛋白基因突变可能建议传染性在细胞的影响。磷酸化也保护内皮障碍对LPS内毒素,暗示它是一个目标对肺药物开发水肿和急性呼吸窘迫综合征(ARDS)。

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