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Related Concept Videos

The Slice Culture Method for Following Development of Tooth Germs In Explant Culture07:47

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Related Experiment Video

Updated: Jan 19, 2026

The Slice Culture Method for Following Development of Tooth Germs In Explant Culture
07:47

The Slice Culture Method for Following Development of Tooth Germs In Explant Culture

Published on: November 13, 2013

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Smad7 Regulates Dental Epithelial Proliferation during Tooth Development.

Z Liu1,2,3, T Chen1,2,4, D Bai1,4

  • 1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, West China Hospital of Stomatology, Sichuan University, Chengdu, P.R. China.

Journal of Dental Research
|September 10, 2019
PubMed
Summary

Smad7 deficiency severely compromises tooth size by inhibiting dental epithelial cell proliferation. This occurs through the hyperactivation of transforming growth factor-β (TGF-β) signaling, highlighting Smad7

Keywords:
TGF-β signalingcell proliferationdental epitheliumnegative modulatortooth morphogenesistooth size

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Related Experiment Videos

Last Updated: Jan 19, 2026

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Tooth morphogenesis requires precise regulation of cell proliferation and differentiation.
  • Transforming growth factor-β (TGF-β) signaling is crucial in tooth development, but the role of Smad7, a TGF-β signaling antagonist, is unknown.

Purpose of the Study:

  • To investigate the precise role of Smad7 in tooth development and its impact on tooth size.

Main Methods:

  • Analysis of Smad7 expression in developing mouse molars.
  • Studying the effects of Smad7 deficiency on tooth size and cell proliferation.
  • RNA sequencing (RNA-seq) to analyze gene expression changes.
  • In vitro culture of Smad7-deficient molar tooth germs with TGF-β signaling inhibitors.

Main Results:

  • Smad7 deficiency led to reduced tooth size due to compromised dental epithelial cell proliferation.
  • Smad7 ablation downregulated genes involved in epithelial cell proliferation and G1/S phase transition.
  • Upregulated genes in Smad7-deficient teeth were associated with TGF-β signaling and cell cycle arrest, including increased Cdkn1a (p21) and decreased Ccnd1 (cyclin D1).
  • Hyperactivation of canonical TGF-β signaling (elevated p-Smad2/3) was observed in Smad7 null mice.
  • Inhibiting TGF-β signaling in vitro rescued cyclin D1 expression and cell proliferation in Smad7-deficient tooth germs.

Conclusions:

  • Smad7 acts as a positive regulator of cell proliferation in dental epithelium development.
  • Smad7 inhibits canonical TGF-β signaling, thereby controlling tooth size.
  • Smad7 plays a crucial role in regulating tooth size during development.