Plasminogen activator inhibitor type 1 expression induced by lipopolysaccharide of Porphyromonas gingivalis in human gingival fibroblast

J Microbiol. 2014 Feb;52(2):154-60. doi: 10.1007/s12275-014-3022-7. Epub 2014 Feb 1.

Abstract

In the gingival tissues of patients with periodontitis, inflammatory responses are mediated by a wide variety of genes. In our previous screening study, plasminogen activator inhibitor type 1 (PAI-1) mRNA binding protein expression was increased in gingiva from periodontitis patients. In this study, we further investigated the signaling pathway involved in PAI-1 expression induced by Porphyromonas gingivalis LPS (Pg LPS) in human gingival fibroblasts (HGF). When HGFs were treated with Pg LPS, both PAI-1 mRNA expression and PAI-1 protein were induced in a dose-dependent manner. Pg LPS induced NF-κB activation and the expressions of PAI-1 mRNA and protein were suppressed by pretreating with a NF-κB inhibitor. Pg LPS also induced ERK, p38, and JNK activation, and Pg LPS-induced PAI-1 expression was inhibited by ERK/p38/JNK inhibitor pretreatment. In conclusion, Pg LPS induced PAI-1 expression through NF-κB and MAP kinases activation in HGF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Body Fluids / cytology
  • Body Fluids / metabolism
  • Cell Line
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Gingiva / chemistry
  • Gingiva / cytology*
  • Humans
  • Lipopolysaccharides / pharmacology*
  • Plasminogen Activator Inhibitor 1 / analysis
  • Plasminogen Activator Inhibitor 1 / genetics
  • Plasminogen Activator Inhibitor 1 / metabolism*
  • Porphyromonas gingivalis / chemistry*

Substances

  • Lipopolysaccharides
  • Plasminogen Activator Inhibitor 1
  • Extracellular Signal-Regulated MAP Kinases