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Updated: Jun 10, 2026

In Vitro Culture of Epicardial Cells From Mouse Embryonic Heart
Published on: April 27, 2016
Role of fibroblast growth factor signaling during proepicardium formation in the chick embryo
Angela Torlopp1, Jan Schlueter, Thomas Brand
1Cell and Developmental Biology, University of Würzburg, Germany.
Insights
Fibroblast growth factors (FGFs) are crucial for embryonic proepicardium development, promoting cell survival and outgrowth. However, FGF signaling does not influence the expression of key proepicardium marker genes.
Area of Science:
- Developmental biology
- Cardiovascular research
- Cell signaling
Background:
- The proepicardium is a transient structure at the embryonic heart's venous pole.
- It serves as a source for multiple mature heart cell types.
- The role of fibroblast growth factors (FGFs) in its development is not fully understood.
Purpose of the Study:
- To investigate the function of FGF signaling in proepicardium formation.
- To determine the impact of FGFs on proepicardium cell proliferation, survival, and gene expression.
Main Methods:
- Expression analysis of FGF ligands and receptors in the embryonic chick proepicardium.
- Experimental modulation of FGF signaling using explant cultures and in vivo studies.
- Assessment of cell proliferation, survival, and expression of specific marker genes (Tbx18, Wt1, Tbx5).
Main Results:
- FGF ligands and receptors are expressed in the proepicardium.
- FGF signaling inhibition reduced cell proliferation and survival in explant cultures.
- In vivo, FGF inhibition impaired proepicardium villous outgrowth but maintained Tbx18 expression.
- Expression of Tbx18, Wt1, and Tbx5 remained unaffected by FGF inhibition.
Conclusions:
- FGFs act as autocrine or paracrine factors essential for proepicardium cell proliferation, survival, and villous outgrowth.
- FGF signaling is not required for the induction or maintenance of proepicardium-specific gene expression.
Abstract:
The proepicardium forms at the venous pole of the embryonic heart and gives rise to several cell types of the mature heart. We investigated the role of fibroblast growth factors (FGFs) during proepicardium formation in the chick embryo. Several FGF ligands (Fgf2, Fgf10, and Fgf12) and receptors (Fgfr1, Fgfr2, and Fgfr4) are expressed in the proepicardium. Experimental modulation of FGF signaling in explant cultures affected cell proliferation and survival. In contrast, expression of Tbx18, Wt1, or Tbx5 were unaffected by FGF inhibition. In agreement with the explant data, villous outgrowth of the proepicardium was strongly impaired by FGF inhibition in vivo, however Tbx18 expression was maintained. These data suggest that during proepicardium formation, FGF ligands act as autocrine or paracrine growth factors to prevent apoptosis, maintain proliferation, and to promote villous outgrowth of the proepicardium. However, FGF is not involved in the induction or maintenance of proepicardium-specific marker gene expression.
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