title: p38a MAPK is involved in BMP-2-induced odontoblastic differentiation of human dental pulp cells.
abstract: OBJECTIVE
  To investigate whether the p38α mitogen-activated protein kinases (MAPK) is involved in bone morphogenetic protein (BMP)-2-induced odontoblastic differentiation of human dental pulp cells (HDPCs).
  
  
  METHODS
  Recombinant retrovirus encoding shRNA against p38α MAPK was constructed to investigate the role of p38α MAPK on BMP-2-induced odontoblastic differentiation of HDPCs. HDPCs were transfected with retrovirus expressing sh-p38α. Activation of p38α MAPK was detected by Western blot. The effects of p38α MAPK on BMP-2-induced odontoblastic differentiation of HDPCs were measured by alkaline phosphatase (ALP) activity, and the expression of odontoblastic markers was identified by quantitative real-time polymerase chain reaction analysis. The effect of SD-282, a p38a-specific inhibitor, on BMP-2-induced odontoblastic differentiation was also investigated.
  
  
  RESULTS
  BMP-2 dose- and time-dependently upregulated phosphorylation of p38α of HDPCs. Compared with BMP-2-treatment group, gene knock-down of p38α MAPK significantly inhibited ALP activity and the formation of mineralized nodules in HDPCs. Moreover, suppression of p38α MAPK repressed the odontoblastic differentiation in HDPCs. Consistently, inhibition of p38α by SD-282 also decreased odontoblastic differentiation.
  
  
  CONCLUSIONS
  p38α MAPK is involved in BMP-2-induced odontoblastic differentiation of HDPCs.
authors: Department of Operative Dentistry and Endodontics, Guanghua School and Hospital of Stomatology & Institute of Stomatological Research, Sun Yat-sen University, Guangzhou, China.
authors: W
authors: W
authors: Qin
authors: Z M
authors: ZM
authors: Lin
authors: R
authors: R
authors: Deng
authors: D D
authors: DD
authors: Li
authors: Z
authors: Z
authors: Song
authors: Y G
authors: YG
authors: Tian
authors: R F
authors: RF
authors: Wang
authors: J Q
authors: JQ
authors: Ling
authors: X F
authors: XF
authors: Zhu
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000032:analysis; D015153:Blotting, Western; D055396:Bone Morphogenetic Protein 2 / Q000187:drug effects / Q000502:physiology*; D002113:Calcification, Physiologic / Q000187:drug effects; D018929:Cell Culture Techniques; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D003782:Dental Pulp / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology; D019084:Fluorescent Antibody Technique, Indirect; D055785:Gene Knockdown Techniques; D020868:Gene Silencing; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D048308:Mitogen-Activated Protein Kinase 14 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D009804:Odontoblasts / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D010766:Phosphorylation; D034741:RNA, Small Interfering / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D012190:Retroviridae / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection; D015854:Up-Regulation / Q000187:drug effects
chemical_list: C525718:BMP2 protein, human; D055396:Bone Morphogenetic Protein 2; D007211:Indoles; D034741:RNA, Small Interfering; C514526:indole-5-carboxamide; D048308:Mitogen-Activated Protein Kinase 14; D000469:Alkaline Phosphatase