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Updated: Jun 2, 2026

Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney
Published on: April 22, 2011
p120 catenin is required for normal renal tubulogenesis and glomerulogenesis
Denise K Marciano1, Paul R Brakeman, Chao-Zong Lee
1Department of Medicine, University of California, San Francisco, CA 94158, USA. denise.marciano@utsouthwestern.edu
Abstract:
Defects in the development or maintenance of tubule diameter correlate with polycystic kidney disease. Here, we report that absence of the cadherin regulator p120 catenin (p120ctn) from the renal mesenchyme prior to tubule formation leads to decreased cadherin levels with abnormal morphologies of early tubule structures and developing glomeruli. In addition, mutant mice develop cystic kidney disease, with markedly increased tubule diameter and cellular proliferation, and detached luminal cells only in proximal tubules. The p120ctn homolog Arvcf is specifically absent from embryonic proximal tubules, consistent with the specificity of the proximal tubular phenotype. p120ctn knockdown in renal epithelial cells in 3D culture results in a similar cystic phenotype with reduced levels of E-cadherin and active RhoA. We find that E-cadherin knockdown, but not RhoA inhibition, phenocopies p120ctn knockdown. Taken together, our data show that p120ctn is required for early tubule and glomerular morphogenesis, as well as control of luminal diameter, probably through regulation of cadherins.
Insights
Absence of p120 catenin (p120ctn) in developing kidneys causes abnormal tubule and glomeruli formation, leading to polycystic kidney disease. This cadherin regulator is crucial for controlling tubule diameter and kidney development.
Area of Science:
- Nephrology
- Developmental Biology
- Cell Biology
Background:
- Polycystic kidney disease (PKD) is linked to defects in renal tubule diameter regulation.
- Cadherin regulators play a role in maintaining epithelial structure and function.
Purpose of the Study:
- To investigate the role of p120 catenin (p120ctn) in early kidney development and its potential link to polycystic kidney disease.
- To elucidate the molecular mechanisms by which p120ctn influences tubule morphogenesis and diameter control.
Main Methods:
- Utilized a mouse model with conditional deletion of p120ctn in the renal mesenchyme.
- Performed p120ctn knockdown in renal epithelial cells cultured in 3D.
- Analyzed kidney morphology, tubule diameter, cellular proliferation, and cadherin/RhoA levels.
Main Results:
- Absence of p120ctn led to decreased cadherin levels, abnormal early tubule and glomerular structures.
- Mutant mice developed cystic kidney disease with increased tubule diameter and proliferation, specifically in proximal tubules.
- p120ctn knockdown in vitro phenocopied the cystic phenotype, with reduced E-cadherin and active RhoA, and E-cadherin knockdown mimicked these effects.
Conclusions:
- p120ctn is essential for proper early tubule and glomerular morphogenesis.
- p120ctn regulates renal tubule diameter, likely via controlling cadherin levels.
- These findings highlight p120ctn as a critical factor in kidney development and a potential therapeutic target for polycystic kidney disease.
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