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Updated: Jun 9, 2026
08:57
En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
Published on: July 27, 2022
Adam10 is essential for early embryonic cardiovascular development.
Chi Zhang1, Lei Tian, Congwu Chi
1Institute of Developmental Biology and Molecular Medicine, School of Life Sciences, Fudan University, Shanghai, China.
Summary
Adam10 is essential for cardiovascular development, regulating the Notch pathway in endothelial cells. Its absence causes embryonic death with cardiac and vascular defects, highlighting its critical role.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- The Notch pathway is crucial for cardiovascular development.
- Receptor cleavage releases an intracellular fragment to activate downstream genes.
- Adam10's role in Notch-mediated cardiovascular development is unclear.
Purpose of the Study:
- To investigate the physiological function of Adam10 in vascular and cardiac development.
- To determine if Adam10 is required for Notch pathway activation in cardiovascular development.
Main Methods:
- Generated mice lacking the Adam10 gene in endothelial cells.
- Observed embryonic lethality and cardiac/vascular defects.
- Analyzed expression of Notch target genes (Snail, Bmp2) in mutant tissues.
Main Results:
- Adam10 deficiency in endothelial cells led to embryonic death post-E10.5.
- Mutant embryos exhibited cardiac and vascular defects, similar to Notch1 mutants.
- Expression of Snail and Bmp2 was impaired in Adam10-deficient cardiac tissues.
Conclusions:
- Adam10 is essential for mammalian cardiac development.
- Adam10 acts autonomously within endothelial cells to regulate cardiovascular development via the Notch pathway.
- Adam10 is required for the activation of Notch target genes during cardiovascular development.
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