title: L-mimosine and dimethyloxaloylglycine decrease plasminogen activation in periodontal fibroblasts.
abstract: BACKGROUND
  The use of prolyl hydroxylase inhibitors such as l-mimosine (L-MIM) and dimethyloxaloylglycine (DMOG) to improve angiogenesis is a new approach for periodontal regeneration. In addition to exhibiting pro-angiogenic effects, prolyl hydroxylase inhibitors can modulate the plasminogen activator system in cells from non-oral tissues. This study assesses the effect of prolyl hydroxylase inhibitors on plasminogen activation by fibroblasts from the periodontium.
  
  
  METHODS
  Gingival and periodontal ligament fibroblasts were incubated with L-MIM and DMOG. To investigate whether prolyl hydroxylase inhibitors modulate the net plasminogen activation, kinetic assays were performed with and without interleukin (IL)-1. Moreover, plasminogen activators and the respective inhibitors were analyzed by casein zymography, immune assays, and quantitative polymerase chain reaction.
  
  
  RESULTS
  The kinetic assay showed that L-MIM and DMOG reduced plasminogen activation under basal and IL-1-stimulated conditions. Casein zymography revealed that the effect of L-MIM involves a decrease in urokinase-type plasminogen activator activity. In agreement with these findings, reduced levels of urokinase-type plasminogen activator and elevated levels of plasminogen activator inhibitor 1 were observed.
  
  
  CONCLUSIONS
  L-MIM and DMOG can reduce plasminogen activation by fibroblasts from the gingiva and the periodontal ligament under basal conditions and in the presence of an inflammatory cytokine.
authors.affiliation: Department of Oral Surgery, Medical University of Vienna, Vienna, Austria.
authors.forename: Christian
authors.initials: C
authors.lastname: Wehner
authors.forename: Reinhard
authors.initials: R
authors.lastname: Gruber
authors.forename: Hermann
authors.initials: H
authors.lastname: Agis
mesh_terms: D000293:Adolescent; D000600:Amino Acids, Dicarboxylic / Q000494:pharmacology*; D018929:Cell Culture Techniques; D002478:Cells, Cultured; D005260:Female; D005347:Fibroblasts / Q000187:drug effects*; D005881:Gingiva / Q000166:cytology / Q000187:drug effects; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D008297:Male; D008898:Mimosine / Q000494:pharmacology*; D010513:Periodontal Ligament / Q000166:cytology* / Q000187:drug effects; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D010960:Plasminogen Activators / Q000494:pharmacology; D015849:Plasminogen Inactivators / Q000494:pharmacology*; D064800:Prolyl-Hydroxylase Inhibitors / Q000494:pharmacology; D014568:Urokinase-Type Plasminogen Activator / Q000037:antagonists & inhibitors
chemical_list: D000600:Amino Acids, Dicarboxylic; D007375:Interleukin-1; D017395:Plasminogen Activator Inhibitor 1; D015849:Plasminogen Inactivators; D064800:Prolyl-Hydroxylase Inhibitors; C051321:SERPINE1 protein, human; D008898:Mimosine; D010960:Plasminogen Activators; D014568:Urokinase-Type Plasminogen Activator; C040947:oxalylglycine