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Updated: Jun 16, 2026
09:58
A Method for Labeling Vasculature in Embryonic Mice
Published on: October 7, 2011
p120-Catenin is required for mouse vascular development.
Rebecca G Oas1, Kanyan Xiao, Susan Summers
1Department of Cell Biology, 615 Michael St, Room 465, Atlanta, GA 30322, USA.
Circulation Research
|January 30, 2010
Summary
p120-catenin is essential for blood vessel development. Its absence in endothelial cells disrupts cadherin levels, leading to vascular disorganization, hemorrhaging, and embryonic lethality.
Area of Science:
- Cell Biology
- Developmental Biology
- Vascular Biology
Background:
- p120-catenin (p120) is an armadillo protein that binds classical cadherins.
- p120 inhibits cadherin endocytosis.
- The function of p120 in vascular development is not understood.
Purpose of the Study:
- To investigate the role of p120 in mammalian vascular development.
- To create a mouse model with endothelial-specific p120 knockout.
- To assess the impact on vasculogenesis, angiogenesis, and cadherin regulation.
Main Methods:
- Utilized a Cre/loxP conditional gene deletion system.
- Employed the Tie2 promoter for endothelial Cre recombinase expression.
- Generated and analyzed mice lacking endothelial p120.
Main Results:
- Endothelial p120 knockout mice exhibited embryonic lethality by E11.5.
- Mutant vasculature showed disorganization and reduced microvascular density.
- Vascular endothelial cadherin and N-cadherin levels were decreased, leading to hemorrhaging and impaired pericyte recruitment.
- p120-null endothelial cells displayed proliferation defects.
Conclusions:
- p120 is crucial for regulating endothelial cadherin levels during vascular development.
- p120 is vital for microvascular patterning, vessel integrity, and endothelial cell proliferation.
- Loss of endothelial p120 causes embryonic lethality due to vascular defects.
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