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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.
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Related Experiment Video

Updated: Aug 23, 2025

In Vitro Culture of Epicardial Cells From Mouse Embryonic Heart
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CCBE1 Is Essential for Epicardial Function during Myocardium Development.

Fernando Bonet1,2, Sabrina Brito Añez1, José Manuel Inácio1

  • 1Stem Cells and Development Laboratory, iNOVA4Health, NOVA Medical School/Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, 1169-056 Lisbon, Portugal.

International Journal of Molecular Sciences
|October 27, 2022
PubMed
Summary

CCBE1 is crucial for epicardial development and function. Loss of CCBE1 in mice causes congenital heart defects by disrupting epicardial cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT).

Keywords:
CCBE1EMTepicardial derived cellsepicardiumheart developmentmyocardial growth

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The Isolation and Culture of Primary Epicardial Cells Derived from Human Adult and Fetal Heart Specimens
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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • The epicardium, a mesothelial cell layer, is vital for heart development, providing cells and growth factors.
  • CCBE1, an extracellular matrix protein from epicardial cells, is known to be essential for coronary plexus formation.

Purpose of the Study:

  • To investigate the role of CCBE1 during epicardial development.
  • To understand the impact of CCBE1 deficiency on heart development and function.

Main Methods:

  • Utilized a Ccbe1 knockout (KO) mouse model.
  • Performed epicardial outgrowth culture assays to assess epicardial-derived cell migration.
  • Analyzed gene expression using RNA-sequencing (RNA-seq) and quantitative real-time PCR (qRT-PCR).

Main Results:

  • Ccbe1 KO mice exhibited congenital heart defects, including thinner, hyper-trabeculated ventricular myocardium.
  • Loss of CCBE1 led to reduced proliferation of cardiomyocytes and epicardial cells, and impaired epicardial-derived cell migration.
  • Ccbe1 deficiency resulted in fewer intramyocardial nonmyocyte/nonendothelial cells and deregulation of epithelial-to-mesenchymal transition (EMT)-related genes.

Conclusions:

  • CCBE1 is essential for normal epicardial development and function.
  • Myocardial defects in Ccbe1 KO mice are attributed to the disruption of epicardial development and associated processes like EMT.