title: Porphyromonas gingivalis antigens and interleukin-6 stimulate the production of monocyte chemoattractant protein-1 via the upregulation of early growth response-1 transcription in human coronary artery endothelial cells.
abstract: BACKGROUND
  Individuals with periodontitis have elevated serum levels of IL-6 and C-reactive protein and have been reported to have a significantly increased risk of developing cardiovascular disease. The transcription factor early growth response factor 1 (Egr-1) has been shown to play an important role in the development and progression of atherosclerosis. However, it is not known whether periodontal infection affects the expression of Egr-1 and subsequent endothelial cells expression of monocyte chemoattractant protein (MCP)-1, a key molecule of leukocyte chemoattraction into vessels.
  
  
  METHODS
  Human coronary artery endothelial cells (HCAECs) were stimulated with either sonicated extracts from Porphyromonas gingivalis strains 381 or SU63, or a combination of IL-6 and soluble IL-6 receptor (IL-6/sIL-6R). The expression of Egr-1, and subsequently MCP-1, was then analyzed. The role of Egr-1 on MCP-1 expression was analyzed by siRNA transfection.
  
  
  RESULTS
  Both P. gingivalis antigens and IL-6/sIL-6R stimulations upregulated the expression of Egr-1, with a more robust effect by IL-6/sIL-6R. Increased expression of Egr-1 coincided with MCP-1 production, and Egr-1 downregulation by siRNA suppressed this effect.
  
  
  CONCLUSIONS
  These results clearly suggest that periodontal infection has the potential to affect HCAECs and hence contribute to the development of subsequent atherosclerosis.
authors.affiliation: Center for Transdisciplinary Research, Niigata University, Niigata 951-8514, Japan.
authors.forename: Tomoki
authors.initials: T
authors.lastname: Maekawa
authors.forename: Naoki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Honda
authors.forename: Daisuke
authors.initials: D
authors.lastname: Yonezawa
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Miyashita
authors.forename: Takafumi
authors.initials: T
authors.lastname: Okui
authors.forename: Koichi
authors.initials: K
authors.lastname: Tabeta
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D000942:Antigens, Bacterial / Q000276:immunology*; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D003331:Coronary Vessels / Q000276:immunology* / Q000378:metabolism; D051766:Early Growth Response Protein 1 / Q000235:genetics / Q000378:metabolism*; D042783:Endothelial Cells / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism*; D016966:Porphyromonas gingivalis / Q000276:immunology*; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D019947:Receptors, Interleukin-6 / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D000942:Antigens, Bacterial; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C497325:EGR1 protein, human; D051766:Early Growth Response Protein 1; C508600:IL6 protein, human; C508603:IL6R protein, human; D015850:Interleukin-6; D012333:RNA, Messenger; D019947:Receptors, Interleukin-6; D011994:Recombinant Proteins