title: Basic fibroblast growth factor inhibits osteogenic differentiation of stem cells from human exfoliated deciduous teeth through ERK signaling.
abstract: OBJECTIVE
  Stem cells from human exfoliated deciduous teeth (SHED) are a unique postnatal stem cell population capable of regenerating mineralized tissue and treating immune disorders. However, the mechanism that controls SHED differentiation is not fully understood. Here, we showed that basic fibroblast growth factor (bFGF) treatment attenuated SHED-mediated mineralized tissue regeneration through activation of the extracellular signal-regulated kinase (ERK) 1/2 pathway.
  
  
  METHODS
  The level of mineralized nodule formation was assessed by alizarin red staining. Expression levels of osteogenic genes, osteocalcin and runt-related transcription factor 2, were examined by RT-PCR. Subcutaneous implantation approach was used to assess in vivo bone formation. Downstream signaling pathways of bFGF were examined by Western blotting.
  
  
  RESULTS
  Activation of ERK1/2 signaling by bFGF treatment inhibited WNT/β-catenin pathway, leading to osteogenic deficiency of SHED. ERK1/2 inhibitor treatment rescued bFGF-induced osteogenic differentiation deficiency.
  
  
  CONCLUSIONS
  These data suggest that bFGF inhibits osteogenic differentiation of SHED via ERK1/2 pathway. Blockade ERK1/2 signaling by small molecular inhibitor treatment improves bone formation of SHED after bFGF treatment.
authors.affiliation: Department of Prosthodontics, School of Stomatology, Fourth Military Medical University, Shaanxi, China.
authors.forename: B
authors.initials: B
authors.lastname: Li
authors.forename: C
authors.initials: C
authors.lastname: Qu
authors.forename: C
authors.initials: C
authors.lastname: Chen
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: K
authors.initials: K
authors.lastname: Akiyama
authors.forename: R
authors.initials: R
authors.lastname: Yang
authors.forename: F
authors.initials: F
authors.lastname: Chen
authors.forename: Y
authors.initials: Y
authors.lastname: Zhao
authors.forename: S
authors.initials: S
authors.lastname: Shi
mesh_terms: D050156:Adipogenesis / Q000187:drug effects; D000818:Animals; D001549:Benzamides / Q000494:pharmacology; D002113:Calcification, Physiologic / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D050659:Core Binding Factor Alpha 1 Subunit / Q000187:drug effects; D004159:Diphenylamine / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology*; D006801:Humans; D006882:Hydroxyapatites; D016130:Immunophenotyping; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D051379:Mice; D008819:Mice, Nude; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D015675:Osteocalcin / Q000187:drug effects; D010012:Osteogenesis / Q000187:drug effects*; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000187:drug effects*; D040521:Subcutaneous Tissue / Q000601:surgery; D054457:Tissue Scaffolds; D014094:Tooth, Deciduous / Q000166:cytology*; D060449:Wnt Signaling Pathway / Q000187:drug effects
chemical_list: D001549:Benzamides; D050659:Core Binding Factor Alpha 1 Subunit; D006882:Hydroxyapatites; C493709:RUNX2 protein, human; D016222:Fibroblast Growth Factor 2; D015675:Osteocalcin; C094280:hydroxyapatite-tricalciumphosphate composite; C506614:mirdametinib; D004159:Diphenylamine; D020928:Mitogen-Activated Protein Kinases