Bilirubin reversibly affects cell death and odontogenic capacity in stem cells from human exfoliated deciduous teeth.

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  • Additional Information
    • Source:
      Publisher: Munksgaard Country of Publication: Denmark NLM ID: 9508565 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1601-0825 (Electronic) Linking ISSN: 1354523X NLM ISO Abbreviation: Oral Dis
    • Publication Information:
      Publication: 2001- : Copenhagen, Denmark : Munksgaard
      Original Publication: Houndmills, Basingstoke, Hampshire, UK : Stockton Press, c1995-
    • Subject Terms:
      Stem Cells*; Bilirubin/*pharmacology ; Cell Death/*drug effects ; Odontogenesis/*drug effects ; Tooth, Deciduous/*cytology; Biliary Atresia/blood ; Cell Proliferation/drug effects ; Cells, Cultured ; Child, Preschool ; Humans ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Tooth Exfoliation ; Transcription Factor RelA/metabolism
    • Abstract:
      Objective: Hyperbilirubinemia in patients with biliary atresia causes deciduous tooth injuries such as green pigmentation and dentin hypoplasia. In patients with biliary atresia who received liver transplantation, tooth structure appears to be recovered radiographically. Nevertheless, little is known about cellular mechanisms underlying bilirubin-induced damage and suppression of deciduous tooth formation. In this study, we examined the effects of bilirubin in stem cells from human exfoliated deciduous teeth (SHED) in vitro.
      Materials and Methods: SHED were cultured under exposure to excess of bilirubin and then interruption of bilirubin stimulation.
      Results: Bilirubin induced cell death and inhibited the odontogenic capacity of SHED by suppressing AKT and extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathways and enhancing nuclear factor kappa B p65 (NF-κB p65) pathway. The interruption of bilirubin stimulation reduced cell death and recovered the inhibited odontogenic capacity of bilirubin-damaged SHED. The bilirubin interruption also normalized the impaired AKT, ERK1/2, and NF-κB p65 signaling pathways.
      Conclusion: These findings suggest that tooth hypodontia in patients with hyperbilirubinemia might be due to bilirubin-induced cell death and dentinogenic dysfunction of odontogenic stem cells via AKT, ERK1/2, and NF-κB pathways and also suggested that bilirubin-induced impairments in odontogenic stem cells were reversible when bilirubin stimulation is interrupted.
      (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. All rights reserved.)
    • Contributed Indexing:
      Keywords: biliary atresia; dentin hypoplasia; hyperbilirubinemia; liver transplantation; stem cells from exfoliated deciduous teeth
    • Accession Number:
      0 (Transcription Factor RelA)
      EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
      EC 2.7.11.24 (MAPK1 protein, human)
      EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
      EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
      RFM9X3LJ49 (Bilirubin)
    • Publication Date:
      Date Created: 20180110 Date Completed: 20181107 Latest Revision: 20181107
    • Publication Date:
      20231215
    • Accession Number:
      10.1111/odi.12827
    • Accession Number:
      29316063