IFT80 is required for stem cell proliferation, differentiation, and odontoblast polarization during tooth development

Xue Yuan, Xu Cao, Shuying Yang

Research output: Contribution to journalArticle

Abstract

Primary cilia and intraflagellar transport (IFT) proteins control a wide variety of processes during tissue development and homeostasis. However, their role in regulation of stem cell properties during tooth development remains elusive. Here, we revealed that dental pulp stem cells (DPSCs) express IFT80, which is required for maintaining DPSC properties. Mice with deletion of IFT80 in odontoblast lineage show impaired molar root development and delayed incisor eruption through reduced DPSC proliferation and differentiation, and disrupted odontoblast polarization. Impaired odontoblast differentiation resulted from disrupted hedgehog (Hh) signaling pathways. Decreased DPSC proliferation is associated with impaired fibroblast growth factor 2 (FGF2) signaling caused by loss of IFT80, leading to the disruption of FGF2-FGFR1-PI3K-AKT signaling in IFT80-deficient DPSCs. The results provide the first evidence that IFT80 controls tooth development through influencing cell proliferation, differentiation, and polarization, and Hh and FGF/AKT signaling pathways, demonstrating that IFT proteins are likely to be the new therapeutic targets for tooth and other tissue repair and regeneration.

Original languageEnglish (US)
Article number63
JournalCell Death and Disease
Volume10
Issue number2
DOIs
StatePublished - Feb 1 2019

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Odontoblasts
Dental Pulp
Cell Differentiation
Tooth
Stem Cells
Cell Proliferation
Hedgehogs
Fibroblast Growth Factor 2
Carrier Proteins
Cilia
Incisor
Phosphatidylinositol 3-Kinases
Regeneration
Homeostasis

ASJC Scopus subject areas

  • Immunology
  • Cellular and Molecular Neuroscience
  • Cell Biology
  • Cancer Research

Cite this

IFT80 is required for stem cell proliferation, differentiation, and odontoblast polarization during tooth development. / Yuan, Xue; Cao, Xu; Yang, Shuying.

In: Cell Death and Disease, Vol. 10, No. 2, 63, 01.02.2019.

Research output: Contribution to journalArticle

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