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Updated: Oct 27, 2025
08:57
En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
Published on: July 27, 2022
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Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of
Siyeon Rhee1, David T Paik2,3,4, Johnson Y Yang2,3,4
1Department of Biology, Stanford University, Stanford, CA 94305, USA.
European Heart Journal
|July 19, 2021
Summary
Genetic defects in Ino80 disrupt coronary vessels, leading to non-compaction cardiomyopathy. Specific angiocrine factors from endothelial cells influence cardiomyocyte growth and maturation in this condition.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Genetics
Background:
- Non-compaction cardiomyopathy (NCCM) is a genetic heart muscle disease with poorly understood mechanisms.
- Endothelial cell-specific deletion of Ino80 causes defective coronary vessel development and ventricular non-compaction in mice.
Purpose of the Study:
- Identify angiocrine factors from endocardial and endothelial cells in wildtype and Ino80-deficient embryonic mouse hearts.
- Investigate the impact of these factors on cardiomyocyte proliferation and maturation.
Main Methods:
- Single-cell RNA-sequencing was employed to analyze endothelial and endocardial cells.
- Dysregulated angiocrine factors were identified and their effects on cardiomyocytes assessed.
Main Results:
- A pathological endocardial cell population was observed in non-compacted hearts.
- Downregulation of Col15a1 impaired cardiomyocyte proliferation.
- Upregulation of Tgfbi, Igfbp3, Isg15, and Adm decreased proliferation and increased cardiomyocyte maturation.
Conclusions:
- Coronary endothelial cells normally secrete factors promoting myocardial compaction.
- Pathological endocardial and endothelial cells can secrete factors contributing to NCCM.
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