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Updated: Jun 5, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-&#946; Signaling
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Published on: August 3, 2018

BMP-2 and TGFβ2 shared pathways regulate endocardial cell transformation.

Todd A Townsend1, Jamille Y Robinson, Christopher R Deig

  • 1Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tenn., USA.

Cells, Tissues, Organs
|January 8, 2011
PubMed
Summary
This summary is machine-generated.

Transforming growth factor-β receptor 3 (TGFβR3) regulates heart valve formation by controlling endocardial cell epithelial-mesenchymal transformation (EMT). This process requires Smad4 and the Par6/Smurf1 pathway for TGFβ2 or BMP-2 signaling.

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TGF-&#946;-mediated Endothelial to Mesenchymal Transition (EndMT) and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
07:05

TGF-β-mediated Endothelial to Mesenchymal Transition (EndMT) and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Molecular Signaling

Background:

  • Valvular heart disease poses significant mortality and morbidity risks.
  • Understanding heart valve formation and remodeling is crucial for therapeutic development.
  • Epithelial-mesenchymal transformation (EMT) of endocardial cells in the atrioventricular cushion (AVC) is vital for valve development.

Purpose of the Study:

  • To investigate the downstream signaling mechanisms of type III transforming growth factor-β receptor (TGFβR3) in AVC endocardial cell EMT.
  • To elucidate the roles of Smad and Par6/Smurf1 pathways in TGFβR3-dependent EMT.

Main Methods:

  • Utilized in vitro endocardial cell EMT models.
  • Employed gene targeting (e.g., Smad4, ALK5, Par6, Smurf1) to assess pathway requirements.
  • Investigated responses to TGFβ2 and BMP-2 stimulation.

Main Results:

  • Smad signaling, mediated by Smad4, is essential for AVC EMT and TGFβR3-dependent EMT induced by TGFβ2 or BMP-2.
  • Smads 1, 2, 3, and 5 are required for AVC EMT, but Smad1 or Smad3 overexpression alone does not induce EMT.
  • Inhibition of ALK5, Par6, or Smurf1 significantly blocked EMT, indicating their requirement downstream of TGFβR3 and involvement in tight junction dissolution.

Conclusions:

  • TGFβR3-dependent endocardial cell EMT, stimulated by TGFβ2 or BMP-2, necessitates Smad4.
  • The Par6/Smurf1 pathway is activated downstream of TGFβR3 and is critical for this EMT process.
  • These findings provide insight into molecular mechanisms regulating heart valve development and potential therapeutic targets.