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Updated: May 22, 2026

In Vitro Generation of Heart Field-specific Cardiac Progenitor Cells
Published on: July 3, 2019
Wnt5a and Wnt11 are essential for second heart field progenitor development
Ethan David Cohen1, Mayumi F Miller, Zichao Wang
1Department of Medicine, Division of Endocrinology, University of Rochester, Rochester, NY 14642, USA. ethan_cohen@urmc.rochester.edu
Wnt5a and Wnt11 are crucial for second heart field development. These non-canonical Wnt ligands restrain Wnt/β-catenin signaling, preventing inhibition of cardiac progenitor development.
Area of Science:
- Developmental Biology
- Molecular Biology
- Cardiovascular Research
Background:
- Wnt/β-catenin signaling exhibits a biphasic role in cardiogenesis, initially promoting cardiac progenitor induction but subsequently inhibiting differentiation.
- Previous studies indicated Wnt/β-catenin signaling is essential for second heart field (SHF) development, yet prolonged signaling inhibits SHF progenitor differentiation.
Purpose of the Study:
- To investigate the role of non-canonical Wnt ligands, specifically Wnt5a and Wnt11, in regulating second heart field development.
- To elucidate the mechanism by which Wnt5a and Wnt11 interact with Wnt/β-catenin signaling during cardiac progenitor development.
Main Methods:
- Utilized mouse models to study the effects of Wnt5a and Wnt11 loss on SHF progenitor development.
- Investigated the impact of Wnt5a and Wnt11 on Wnt/β-catenin signaling activity.
- Examined the effects of ectopic Wnt5a/Wnt11 on cardiac progenitor development in differentiating embryonic stem cells.
Main Results:
- Co-deletion of Wnt5a and Wnt11 resulted in a significant loss of second heart field progenitors in developing mouse hearts.
- Loss of Wnt5a and Wnt11 was associated with increased Wnt/β-catenin signaling activity.
- Ectopic expression of Wnt5a and Wnt11 inhibited β-catenin signaling and promoted cardiac progenitor development.
Conclusions:
- Wnt5a and Wnt11 are essential regulators of second heart field development in mice.
- These non-canonical Wnt ligands function by restraining excessive Wnt/β-catenin signaling, thereby promoting cardiac progenitor development.
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