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mTORC1 promotes mineralization via p53 pathway.

Xinghong Luo1,2, Jingyao Yin1,2, Shenghong Miao1,2

  • 1Department of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|January 28, 2021
PubMed
Summary

The mechanistic target of rapamycin complex 1 (mTORC1) pathway promotes odontoblast proliferation and dentin mineralization. This process involves mTORC1 signaling through the p53 pathway, highlighting a novel therapeutic target for dentin repair.

Keywords:
cell signalingdentinogenesismTORC1molecular biologyodontoblasttooth development

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Dentistry

Background:

  • Odontoblast proliferation and mineralization are crucial for dentin formation and repair.
  • The mechanistic target of rapamycin complex 1 (mTORC1) pathway is a key regulator of cell growth and metabolism.
  • Dysregulation of mTORC1 signaling is implicated in various cellular processes, but its specific role in odontoblast function remains unclear.

Purpose of the Study:

  • To investigate the role of mTORC1 in regulating odontoblast proliferation and mineralization.
  • To elucidate the underlying molecular mechanism by which mTORC1 influences odontoblast mineralization.

Main Methods:

  • In vitro studies using MDPC23 cells treated with rapamycin or short hairpin RNA (shRNA) targeting TSC1 to modulate mTORC1 activity.
  • In vivo studies utilizing TSC1-conditional knockout mice (CKO) and wild-type littermates (WT).
  • Assays included CCK8, flow cytometry, Alizarin red S, ALP staining, qRT-PCR, western blot, H&E staining, immunofluorescence, micro-CT, and transcriptome sequencing.

Main Results:

  • mTORC1 inactivation decreased odontoblast proliferation and downregulated mineralization-related genes and proteins.
  • mTORC1 overactivation enhanced proliferation and promoted mineralization markers.
  • In vivo, CKO mice exhibited increased dentin thickness and mineralization compared to WT controls.
  • Transcriptome analysis identified the p53 pathway as a downstream mediator of mTORC1's effects on mineralization.

Conclusions:

  • mTORC1 plays a significant role in promoting odontoblast proliferation and dentin mineralization.
  • mTORC1 upregulates odontoblast mineralization through the p53 signaling pathway.
  • Targeting the mTORC1-p53 axis presents a potential therapeutic strategy for enhancing dentin repair and regeneration.