論文

査読有り
2016年1月

Interferon-gamma improves impaired dentinogenic and immunosuppressive functions of irreversible pulpitis-derived human dental pulp stem cells

SCIENTIFIC REPORTS
  • Soichiro Sonoda
  • Haruyoshi Yamaza
  • Lan Ma
  • Yosuke Tanaka
  • Erika Tomoda
  • Reona Aijima
  • Kazuaki Nonaka
  • Toshio Kukita
  • Songtao Shi
  • Fusanori Nishimura
  • Takayoshi Yamaza
  • 全て表示

6
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/srep19286
出版者・発行元
NATURE PUBLISHING GROUP

Clinically, irreversible pulpitis is treated by the complete removal of pulp tissue followed by replacement with artificial materials. There is considered to be a high potential for autologous transplantation of human dental pulp stem cells (DPSCs) in endodontic treatment. The usefulness of DPSCs isolated from healthy teeth is limited. However, DPSCs isolated from diseased teeth with irreversible pulpitis (IP-DPSCs) are considered to be suitable for dentin/pulp regeneration. In this study, we examined the stem cell potency of IP-DPSCs. In comparison with healthy DPSCs, IP-DPSCs expressed lower colony-forming capacity, population-doubling rate, cell proliferation, multipotency, in vivo dentin regeneration, and immunosuppressive activity, suggesting that intact IP-DPSCs may be inadequate for dentin/pulp regeneration. Therefore, we attempted to improve the impaired in vivo dentin regeneration and in vitro immunosuppressive functions of IP-DPSCs to enable dentin/pulp regeneration. Interferon gamma (IFN-gamma) treatment enhanced in vivo dentin regeneration and in vitro T cell suppression of IP-DPSCs, whereas treatment with tumor necrosis factor alpha did not. Therefore, these findings suggest that IFN-gamma may be a feasible modulator to improve the functions of impaired IP-DPSCs, suggesting that autologous transplantation of IFN-gamma-accelerated IP-DPSCs might be a promising new therapeutic strategy for dentin/pulp tissue engineering in future endodontic treatment.

リンク情報
DOI
https://doi.org/10.1038/srep19286
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000368183000001&DestApp=WOS_CPL
ID情報
  • DOI : 10.1038/srep19286
  • ISSN : 2045-2322
  • Web of Science ID : WOS:000368183000001

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