title: Role of p38 mitogen-activated protein kinase pathway in Porphyromonas gingivalis lipopolysaccharide-induced VCAM-1 expression in human aortic endothelial cells.
abstract: BACKGROUND
  Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) has been reported to induce the expression of vascular cell adhesion molecule-1 (VCAM-1) in vascular endothelial cells. This finding suggests the potential roles for Pg in the pathogenesis of atherosclerosis. However, the mechanism involved in Pg LPS-induced VCAM-1 production in endothelial cells remains unclear.
  
  
  METHODS
  Quantitative real-time polymerase chain reaction and Western blotting were used, respectively, to investigate the mRNA expression and protein production of VCAM-1 in human aortic endothelial cells (HAECs) induced by Pg LPS. The involvement of the p38 mitogen-activated protein kinase (p38 MAPK) cell signaling pathway in VCAM-1 expression was investigated by assays with specific inhibitors.
  
  
  RESULTS
  Pg LPS-induced expression in HAECs of VCAM-1 occurred in a dose- and time-dependent manner. In addition, the p38 MAPK inhibitor (SB 203580) significantly attenuated Pg LPS-induced VCAM-1 expression.
  
  
  CONCLUSIONS
  Activation of p38 MAPK is at least partially involved in Pg LPS-induced VCAM-1 expression in HAECs, which may contribute to the acceleration of atherosclerosis.
authors: Department of Endodontics and Operative Dentistry, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai, China.
authors: Bin
authors: B
authors: Liu
authors: Lan
authors: L
authors: Cheng
authors: DaLi
authors: D
authors: Liu
authors: Jia
authors: J
authors: Wang
authors: XiuLi
authors: X
authors: Zhang
authors: Rong
authors: R
authors: Shu
authors: JingPing
authors: J
authors: Liang
mesh_terms: D001011:Aorta / Q000166:cytology*; D050197:Atherosclerosis / Q000276:immunology; D018929:Cell Culture Techniques; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects* / Q000201:enzymology; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004926:Escherichia coli; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D016966:Porphyromonas gingivalis; D011725:Pyridines / Q000494:pharmacology; D013997:Time Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000187:drug effects*; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors
chemical_list: D004791:Enzyme Inhibitors; D007093:Imidazoles; D008070:Lipopolysaccharides; D011725:Pyridines; D019010:Vascular Cell Adhesion Molecule-1; D048051:p38 Mitogen-Activated Protein Kinases; C093642:SB 203580