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Transforming Growth Factor Beta3 is Required for Cardiovascular Development.

Mrinmay Chakrabarti1, Nadia Al-Sammarraie1, Mengistu G Gebere1

  • 1Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29209, USA.

Journal of Cardiovascular Development and Disease
|May 28, 2020
PubMed
Summary
This summary is machine-generated.

Transforming growth factor beta3 (TGFB3) is essential for proper cardiovascular development. Its absence in mice leads to diverse heart defects, highlighting its role in maintaining TGFβ signaling balance.

Keywords:
arrhythmogenic right ventricular dysplasiacardiac developmentcleft palatecongenital heart diseaseloeys dietz syndrome-5outflow tract septationrienhoff syndromesignaling networkstransforming growth factor beta-3

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • Mutations in Transforming growth factor beta3 (TGFB3) are linked to conditions like arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD1) and Loeys-Dietz syndrome-5 (LDS5).
  • The precise role of TGFB3 in embryonic cardiovascular development and disease remains largely undefined.

Purpose of the Study:

  • To investigate the function of TGFB3 in cardiovascular development and disease using a mouse model.
  • To elucidate the molecular mechanisms underlying TGFB3's role in cardiac formation.

Main Methods:

  • Histological, immunohistochemical, and molecular analyses were performed on TGFB3-deficient (Tgfb3-/-) fetal hearts.
  • In vitro studies utilized TGFB3-deficient fibroblasts in 3-D collagen lattice assays.
  • Biochemical analyses assessed canonical (SMAD-dependent) and noncanonical (MAP kinase-dependent) TGFβ signaling pathways.

Main Results:

  • Approximately two-thirds of Tgfb3-/- fetuses exhibited cardiovascular malformations, including ventricular myocardium abnormalities, outflow tract defects, and valve thickening.
  • Ventricular septal defects (VSDs) were observed in Tgfb3-/- fetuses, often associated with myocardial defects.
  • TGFB3 deficiency impaired collagen matrix reorganization in vitro and led to paradoxical activation of canonical and noncanonical TGFβ signaling pathways.

Conclusions:

  • TGFB3 is crucial for normal cardiovascular development, preventing a range of congenital heart defects.
  • The study demonstrates TGFB3's requirement for maintaining a balance between canonical and noncanonical TGFβ signaling pathways during heart development.