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Endocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in
Rie Saba1,2, Keiko Kitajima3, Lucille Rainbow4
1Centres for Microvascular Research and for Endocrinology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Scientific Reports
|August 18, 2019
Summary
Sox17 expression in cardiac progenitor cells biases differentiation toward the endocardium. Sox17 is crucial for endocardium development and subsequent heart formation, impacting myocardial proliferation and trabeculation.
Area of Science:
- Developmental Biology
- Cardiovascular Biology
- Molecular Biology
Background:
- The endocardium, the heart's endothelial lining, is vital for cardiac development.
- The precise mechanisms of endocardial segregation during embryogenesis are not fully understood.
Purpose of the Study:
- To elucidate the role of Sox17 in endocardial differentiation and heart development.
- To identify the signaling pathways influenced by Sox17 during embryogenesis.
Main Methods:
- Utilized mouse embryos to track cardiac progenitor cell (CPC) differentiation.
- Investigated Sox17 expression patterns and functional requirements using genetic manipulation (deletion).
- Analyzed effects on endocardial and myocardial development, including cell proliferation and signaling pathways.
Main Results:
- Sox17 expression in Nkx2-5+ CPCs from E7.5-E8.5 biases differentiation towards the endocardium.
- Sox17 is essential for endocardium development, affecting cell proliferation and behavior.
- Sox17 deletion impairs cardiomyocyte proliferation, ventricular trabeculation, and myocardium thickening via non-cell-autonomous mechanisms, likely involving NOTCH signaling.
Conclusions:
- Sox17 plays a critical role in endocardial fate specification and is indispensable for proper heart development.
- Sox17 regulates myocardial development through signaling pathways, including NOTCH, highlighting its broader impact on cardiac morphogenesis.
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