title: p38 mitogen-activated protein kinase and alkaline phosphatase in human dental pulp cells.
abstract: OBJECTIVE
  The objective of this study was to investigate the implication of p38 mitogen-activated protein kinase (MAPK) in mediating alkaline phosphatase (ALPase) activity in human dental pulp cells (HPCs).
  
  
  METHODS
  Nuclear translocation of p38 was observed by immunofluorescence in isolated HPCs treated with transforming growth factor beta1 (TGF-beta1). TGF-beta1 was used to examine the interaction between p38 MAPK and Smad pathway. Role of p38 kinase in mediating ALPase activity was determined with SB203580, a specific inhibitor for the p38 pathway. Lipopolysaccharide (LPS) or TGF-beta1 was added to inhibit or increase ALPase activity. Statistical analysis was performed by unpaired t test.
  
  
  RESULTS
  TGF-beta1 induced nuclear translocalization of p38. Blockage of p38 pathway with SB203580 inhibited translocation of Smad2/3 to nuclei. ALPase activity decreased in cells treated with SB203580, in contrast to its vehicle (P < .05). Inhibition on enzyme activity by LPS was exacerbated by SB203580 (P < .05). Treatment with SB203580 before addition of TGF-beta1 also made a significant decrease in ALPase activity (P < .05).
  
  
  CONCLUSIONS
  These results suggest that p38 MAPK is implicated in regulating ALPase activity in HPCs and may interact with Smad pathway.
authors.affiliation: Key Laboratory of Oral Biomedical Engineering, Ministry of Education, Sichuan University, Chengdu, China.
authors.forename: Feng-Ming
authors.initials: FM
authors.lastname: Wang
authors.forename: Tao
authors.initials: T
authors.lastname: Hu
authors.forename: Xuedong
authors.initials: X
authors.lastname: Zhou
mesh_terms: D021581:Active Transport, Cell Nucleus / Q000187:drug effects; D000469:Alkaline Phosphatase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002478:Cells, Cultured; D003782:Dental Pulp / Q000201:enzymology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D011725:Pyridines / Q000494:pharmacology; D011994:Recombinant Proteins / Q000494:pharmacology; D051899:Smad2 Protein / Q000037:antagonists & inhibitors; D051900:Smad3 Protein / Q000037:antagonists & inhibitors; D016212:Transforming Growth Factor beta / Q000494:pharmacology; D053773:Transforming Growth Factor beta1; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology*
chemical_list: D004791:Enzyme Inhibitors; D007093:Imidazoles; D011725:Pyridines; D011994:Recombinant Proteins; D051899:Smad2 Protein; D051900:Smad3 Protein; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D048051:p38 Mitogen-Activated Protein Kinases; D000469:Alkaline Phosphatase; C093642:SB 203580