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Development of the Heart

Development of the Heart

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 tube by...

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Related Experiment Video

Updated: May 19, 2026

Epicardial Outgrowth Culture Assay and Ex Vivo Assessment of Epicardial-derived Cell Migration

Epicardial Outgrowth Culture Assay and Ex Vivo Assessment of Epicardial-derived Cell Migration

Published on: March 18, 2016

Tbx18 function in epicardial development.

Franziska Greulich¹, Henner F Farin, Karin Schuster-Gossler

¹Institut für Molekularbiologie, Medizinische Hochschule Hannover, OE5250, Carl-Neuberg-Str.1, Hannover D-30625, Germany.

Cardiovascular Research

|August 29, 2012

Summary

T-box transcription factor 18 (Tbx18) is not essential for epicardial development. However, Tbx18

Area of Science:

Developmental biology
Cardiovascular research
Gene regulation

Background:

The embryonic epicardium generates coronary vasculature and myocardium.
Molecular mechanisms controlling epicardial cell differentiation are partially understood.

Purpose of the Study:

Investigate the role of the T-box transcription factor Tbx18 in epicardial development.
Elucidate Tbx18's function in generating smooth muscle cells and fibroblasts from epicardial cells.

Main Methods:

Utilized transgenic mouse models to study Tbx18 function.
Performed cellular and molecular analyses on Tbx18-deficient and transgenic mice.
Conducted explant cultures to assess signaling pathway inhibition.

Main Results:

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Tbx18 deficiency did not impair epicardial formation, epithelial-mesenchymal transition, or coronary vasculature development.
Misexpression of an activating Tbx18 variant (Tbx18VP16) induced premature smooth muscle differentiation.
Inhibition of Notch and TGF-β receptor signaling reversed Tbx18VP16-induced differentiation.

Conclusions:

Tbx18 is dispensable for normal epicardial development.
A repressive function of Tbx18 may prevent premature smooth muscle differentiation by regulating Notch and TGF-β signaling.