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Related Concept Videos

Development of the Heart01:27

Development of the Heart

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The development of the human heart, a crucial organ, commences from the mesoderm on the 18th or 19th day after fertilization. This process initiates in the cardiogenic area, a group of mesodermal cells at the embryo's head end, which evolves into elongated strands known as cardiogenic cords. These cords undergo a transformation to form hollow-centered endocardial tubes.
As the embryo undergoes lateral folding, these paired tubes approach each other, merging into a single primitive heart...
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Imaging Cleared Embryonic and Postnatal Hearts at Single-cell Resolution
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14-3-3epsilon controls multiple developmental processes in the mouse heart.

Adriana C Gittenberger-de Groot1,2, Tamara Hoppenbrouwers3, Lucile Miquerol4

  • 1Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands. acgitten@lumc.nl.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|September 1, 2016
PubMed
Summary

Deletion of 14-3-3ε causes severe congenital heart defects, including valve abnormalities and myocardial non-compaction, by disrupting cardiomyocyte cell cycle regulation via p27kip1.

Keywords:
14-3-3cardiac outflow tractcoronary artery hypoplasiaendocardial cushionheart developmentmousemyocardial hypoplasiaventricular septal defect

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • 14-3-3ε is crucial for cardiomyocyte cell cycle modulation via p27kip1 during cardiac maturation.
  • The widespread expression of 14-3-3ε suggests potential roles in various cardiac structures beyond ventricular myocardium.

Purpose of the Study:

  • To investigate the consequences of germ line 14-3-3ε deletion on cardiac development.
  • To elucidate the molecular mechanisms underlying 14-3-3ε-associated cardiac malformations.

Main Methods:

  • Analysis of cardiac phenotypes in germ line 14-3-3ε knockout mouse models.
  • Assessment of p27kip1 expression patterns in developing cardiac tissues.
  • Evaluation of endocardial cushion development, septation, and coronary vasculature formation.

Main Results:

  • Germ line deletion of 14-3-3ε resulted in outflow tract and atrioventricular cushion malalignment, leading to tricuspid stenosis/atresia and mitral valve defects.
  • Observed cardiac defects included perimembranous and muscular ventricular septal defects (VSDs), myocardial non-compaction, and epicardial blebbing.
  • Abnormal p27kip1 patterning, defective pharyngeal arch artery development, deep endocardial recesses, and reduced intramyocardial coronary vasculature were noted.

Conclusions:

  • Endocardial cushion malalignment offers a novel explanation for tricuspid and mitral valve defects.
  • Myocardial non-compaction provides a basis for abnormal coronary vasculature patterning, potentially linked to p27kip1 dysregulation and impaired epithelial-to-mesenchymal transformation.
  • 14-3-3ε deficiency is implicated in various congenital heart diseases (CHDs), including left ventricular non-compaction (LVNC).