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Dkk1 and Dkk2 regulate epicardial specification during mouse heart development.

Matthew D Phillips¹, Mahua Mukhopadhyay, Cristina Poscablo

¹Laboratory of Mammalian Genes and Development, Program in the Genomics of Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, HHS, Bethesda, MD 20892, USA.

International Journal of Cardiology

|May 5, 2010

Summary

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Dickkopf-1 (Dkk1) and Dickkopf-2 (Dkk2) proteins are crucial for heart development. Their combined absence leads to perinatal death and significant cardiac defects, revealing their compensatory roles in regulating Wnt signaling and myocardial proliferation.

Area of Science:

Developmental Biology
Molecular Biology
Cardiovascular Research

Background:

Dkk1 and Dkk2 are Wnt signaling inhibitors crucial for development.
They interact with LRP5/LRP6 receptors to modulate canonical Wnt pathways.
Individual loss-of-function mutations in Dkk1 or Dkk2 do not cause observable heart defects.

Purpose of the Study:

To investigate the combined role of Dkk1 and Dkk2 in embryonic heart development.
To elucidate the function of Dkk1 and Dkk2 in regulating Wnt signaling during cardiac morphogenesis.

Main Methods:

Generation of Dkk1 null and Dkk2 null double mutant mouse embryos.
Histological and immunohistochemical analysis of embryonic hearts at various developmental stages.

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Last Updated: Jun 13, 2026

Imaging Cleared Embryonic and Postnatal Hearts at Single-cell Resolution

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Published on: October 7, 2016

In Vitro Culture of Epicardial Cells From Mouse Embryonic Heart

In Vitro Culture of Epicardial Cells From Mouse Embryonic Heart

Published on: April 27, 2016

Analysis of Cardiac Chamber Development During Mouse Embryogenesis Using Whole Mount Epifluorescence

Analysis of Cardiac Chamber Development During Mouse Embryogenesis Using Whole Mount Epifluorescence

Published on: April 17, 2019

Main Results:

Double null embryos exhibit perinatal lethality and severe head malformations.
Myocardial defects, including ventricular septal defects, are observed in late-stage hearts.
Early stages show myocardial and epicardial hyperplasia, with altered Connexin 43 expression in proepicardial cells.

Conclusions:

Dkk1 and Dkk2 redundantly inhibit Wnt signaling, regulating early myocardial proliferation.
Wnt signaling is essential for myocardial proliferation in both early heart fields.
Wnt signaling influences proepicardial cell specification, potentially contributing to later cardiac defects.