Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2919036 | Heart, Lung and Circulation | 2013 | 7 Pages |
BackgroundOxidised low-density lipoprotein (ox-LDL) led to endothelial dysfunction, which was an initial step in the formation of atheroma. The role of IKKɛ in Ox-LDL-induced endothelial cell injury was investigated in this study.MethodsPrimary cultures of endothelial cell were identified by the immunofluorescent detection of von Willebrand's factor (vWF). Wild-type and IKKɛ knockout endothelial cells were treated with ox-LDL and effects on ultrastructural morphology were evaluated by transmission electron microscopy. Western blotting analysis was conducted to evaluate effects on IL-18, VEGF, IKKα, IKKβ, IKKɛ, p65 and p50 expression.ResultsFrom the ultrastructural morphology of endothelial cells and the expression of inflammatory factor such as IL-18 and VEGF, it was suggested that IKKɛ knockout endothelial cells showed less severe ox-LDL-induced injury compared to wild-type endothelial cells. Ox-LDL increased IKKɛ and phosphorylated IKKɛ expression in wild-type endothelial cells, while no significant change in IKKα and IKKβ levels was observed. Ox-LDL significantly increased the expression of p65(or p50) and phosphorylated p65(or p50) in wild-type endothelial cells, while this effect was completely blocked in IKKɛ knockout endothelial cells.ConclusionsIKKɛ might play an important role in ox-LDL-induced injury of endothelial cells.