title: Vasopressin inhibits mitogen-activated protein kinases and activated protein-1 in macrophages.
abstract: OBJECTIVE
  We have previously shown that vasopressin could inhibit the upregulation of inflammatory mediators. Expression of inflammatory mediators is tightly regulated by the upstream transcriptional pathway mitogen-activated protein kinases (MAPKs) and activated protein-1 (AP-1). In this study, we elucidated whether vasopressin could inhibit the upregulation of MAPKs/AP-1.
  
  
  METHODS
  Murine macrophages (RAW264.7 cells) randomly received lipopolysaccharide (LPS; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL) (designated as the LPS and the LPS+V groups, respectively). Control groups were run simultaneously. For MAPKs, cells were harvested at 0 minutes, 15 minutes, 30 minutes, 45 minutes, and 60 minutes after reaction. For AP-1, cells were harvested at 60 minutes after reaction. Between-group differences in MAPKs (i.e., extracellular regulated kinase, c-Jun N-terminal kinase, and p38 MAPK) and AP-1 expressions were compared.
  
  
  RESULTS
  Immunoblotting assay data revealed that extracellular regulated kinase concentrations of the LPS+V group that harvested at 45 minutes and 60 minutes, but not at 15 minutes and 30 minutes, were significantly lower than those of the LPS group (p=0.005 and p=0.013). C-Jun N-terminal kinase concentrations of the LPS+V group that harvested at 15 minutes, 30 minutes, 45 minutes, and 60 minutes were also significantly lower than those of the LPS group (all p<0.001). Concentrations of p38 MAPK of the LPS+V group that harvested at 15 minutes, 30 minutes, and 45 minutes, but not at 60 minutes, were also significantly lower than those of the LPS group (all p<0.001). In addition, immunohistochemistry assay revealed that the AP-1 fluorescence signals of the LPS+V group were weaker than those of the LPS group.
  
  
  CONCLUSIONS
  Vasopressin inhibits MAPKs and AP-1 in endotoxin-activated macrophages.
authors.affiliation: Department of Emergency Medicine, Taipei Tzu Chi Hospital, Taipei, Taiwan.
authors.forename: Yu-Long
authors.initials: YL
authors.lastname: Chen
authors.affiliation: Department of Anesthesiology, Taipei Tzu Chi Hospital, Taipei, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan.
authors.forename: Ya-Ying
authors.initials: YY
authors.lastname: Chang
authors.affiliation: Department of Anesthesiology, Taipei Tzu Chi Hospital, Taipei, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan.
authors.forename: Ming-Chang
authors.initials: MC
authors.lastname: Kao
authors.affiliation: Department of Anesthesiology, Taipei Tzu Chi Hospital, Taipei, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan. Electronic address: huangcj1112@gmail.com.
authors.forename: Chun-Jen
authors.initials: CJ
authors.lastname: Huang
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects*; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors*; D018808:Transcription Factor AP-1 / Q000037:antagonists & inhibitors*; D014667:Vasopressins / Q000494:pharmacology*
chemical_list: D008070:Lipopolysaccharides; D018808:Transcription Factor AP-1; D014667:Vasopressins; D020928:Mitogen-Activated Protein Kinases
keywords: RAW264.7 cells; activated protein-1; c-Jun N-terminal kinase; extracellular regulated kinase; p38 mitogen-activated protein kinase