title: Effects of IKKɛ on oxidised low-density lipoprotein-induced injury in vascular endothelial cells.
abstract: BACKGROUND
  Oxidised 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.
  
  
  METHODS
  Primary 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.
  
  
  RESULTS
  From 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.
  
  
  CONCLUSIONS
  IKKɛ might play an important role in ox-LDL-induced injury of endothelial cells.
authors.affiliation: Department of Nephrology, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing 210006, China.
authors.forename: Changchun
authors.initials: C
authors.lastname: Cao
authors.forename: Yongchao
authors.initials: Y
authors.lastname: Qi
authors.forename: Wen
authors.initials: W
authors.lastname: Chen
authors.forename: Yifan
authors.initials: Y
authors.lastname: Zhu
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics; D051550:I-kappa B Kinase / Q000235:genetics / Q000378:metabolism*; D020382:Interleukin-18 / Q000096:biosynthesis / Q000235:genetics; D008077:Lipoproteins, LDL / Q000378:metabolism* / Q000494:pharmacology; D051379:Mice; D018345:Mice, Knockout; D052002:NF-kappa B p50 Subunit / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects / Q000235:genetics; D058226:Plaque, Atherosclerotic / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics
chemical_list: D020382:Interleukin-18; D008077:Lipoproteins, LDL; D052002:NF-kappa B p50 Subunit; C498144:Rela protein, mouse; D051996:Transcription Factor RelA; D042461:Vascular Endothelial Growth Factor A; C099252:oxidized low density lipoprotein; C467480:vascular endothelial growth factor A, mouse; C073701:Nfkb1 protein, mouse; D051550:I-kappa B Kinase