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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Smad protein mediated transforming growth factor beta1 induction of apoptosis in the MDPC-23 odontoblast-like cell

Wen-Xi He1, Zhong-Ying Niu, Shou-Liang Zhao

  • 1Department of Conservative Dentistry, Qin Du Stomatological Hospital, School of Dentistry, The Fourth Military Medical University, Xi'an 710032, PR China. hwenxi@yahoo.com.cn

Archives of Oral Biology
|September 27, 2005
PubMed
Abstract

Insights

Transforming growth factor (TGF)-beta 1 induces apoptosis in odontoblast cells. Smad proteins play a crucial role in mediating this TGF-beta1-induced cell death, offering insights into odontoblast regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Dental Research

Background:

  • The role of apoptosis and its regulation in odontoblasts is not fully understood.
  • Transforming growth factor (TGF)-beta 1 is a key signaling molecule with diverse cellular functions.

Purpose of the Study:

  • To investigate the role of TGF-beta 1 in inducing apoptosis in odontoblasts.
  • To elucidate the molecular mechanisms underlying TGF-beta 1-induced apoptosis in odontoblasts, focusing on Smad proteins.

Main Methods:

  • Utilized Annexin V/propidium iodide staining, cell Death Detection ELISA, and DNA ladder assays to assess apoptosis in the mouse odontoblast-like cell line MDPC-23.
  • Generated stable cell clones expressing Smad2 or Smad3 dominant-negative mutants, or wild-type Smad7 to investigate Smad protein involvement.
  • Analyzed TGF-beta 1-induced transcriptional activity using a TGF-beta-responsive reporter gene (p3TP-Lux) in cells expressing Smad proteins.

Main Results:

  • TGF-beta 1 induced apoptosis in MDPC-23 cells in a dose-dependent manner.
  • Dominant-negative mutants of Smad2 and Smad3, particularly Smad3, inhibited TGF-beta 1-induced apoptosis.
  • Smad7 overexpression also significantly inhibited TGF-beta 1-induced apoptosis and transcriptional activity.

Conclusions:

  • Smad proteins are integral to the process of TGF-beta 1-induced apoptosis in odontoblast cells.
  • These findings highlight the involvement of the TGF-beta/Smad signaling pathway in regulating odontoblast cell death.

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