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Cytoskeletal Alterations in Lipopolysaccharide-Induced Bovine Vascular Endothelial Cell Injury and Its Prevention by Sodium Arsenite

机译:脂多糖诱导牛血管内皮细胞损伤中的细胞骨架变化及其亚砷酸钠的预防

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摘要

Morphological changes, especially cytoskeletal alterations, in lipopolysaccharide (LPS)-induced vascular endothelial cell injury were studied by using LPS-susceptible bovine aortic endothelial cells (BAEC). BAEC in cultures with LPS showed cell rounding, shrinking, and intercellular gap formation. In those cells, LPS caused the disorganization of actin, tubulin, and vimentin. LPS also induced a reduction in the F-actin pool and an elevation in the G-actin pool. Cytoskeletal disorganization affected transendothelial permeability across the endothelial monolayer. Pretreatment of BAEC with sodium arsenite (SA) prevented alterations in LPS-induced BAEC injury. However, posttreatment with SA had no protective effect on them. SA upregulated the expression of heat shock protein in the presence of LPS. The role of SA in prevention of LPS-induced BAEC injury is discussed.
机译:使用脂多糖(LPS)敏感的牛主动脉内皮细胞(BAEC)研究了脂多糖(LPS)诱导的血管内皮细胞损伤的形态学变化,尤其是细胞骨架的改变。在具有LPS的培养物中,BAEC显示出细胞变圆,缩小和细胞间间隙形成。在这些细胞中,LPS导致肌动蛋白,微管蛋白和波形蛋白的分解。 LPS还引起F-肌动蛋白池减少和G-肌动蛋白池升高。细胞骨架紊乱影响跨内皮单层的跨内皮通透性。用亚砷酸钠(SA)预处理BAEC可以防止LPS诱导的BAEC损伤的改变。但是,SA的后处理对其没有保护作用。 SA在LPS存在下上调了热激蛋白的表达。讨论了SA在预防LPS引起的BAEC损伤中的作用。

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