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Updated: May 9, 2026
08:03
In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Accelerated coronary angiogenesis by vegfr1-knockout endocardial cells
1The State Key Laboratory of Biotherapy, West China Medical School of Sichuan University, Chengdu, Sichuan, China.
Plos One
|July 30, 2013
Summary
Soluble vascular endothelial growth factor receptor 1 (sVegfr1) normally limits embryonic coronary artery formation. Removing sVegfr1 from endocardial cells accelerates blood vessel development in the mouse heart.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Angiogenesis Research
Background:
- Coronary arteries develop from ventricular endocardial cells via angiogenesis during mouse heart development.
- Myocardially-derived vascular endothelial growth factor-a (Vegfa) signaling through vascular endothelial growth factor-receptor 2 (Vegfr2) on endocardial cells is crucial for this process.
Purpose of the Study:
- To investigate the role of endocardially-produced soluble vascular endothelial growth factor receptor 1 (sVegfr1) in regulating embryonic coronary angiogenesis.
Main Methods:
- Genetic deletion of sVegfr1 in endocardial cells of developing mouse hearts.
- Ex vivo coronary angiogenesis assay using Vegfr1-null ventricular endocardial cells.
- Quantitative PCR (qPCR) analysis of gene expression.
- Inhibition of Notch signaling.
Main Results:
- Deletion of endocardial sVegfr1 led to precocious formation of coronary plexuses.
- Vegfr1-null endocardial cells exhibited excessive angiogenesis and formed extensive endothelial tubular networks in vitro.
- Expression of genes in the vascular endothelial growth factor (Vegf)-Notch pathway was upregulated in Vegfr1-null hearts.
- Notch signaling inhibition blocked coronary plexus formation.
Conclusions:
- Endocardial sVegfr1 acts as a negative regulator of embryonic coronary angiogenesis.
- sVegfr1 may exert its function by modulating the Vegf-Notch signaling pathway.
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