Deletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse

Author:

Thomson R. B.1,Dynia D. W.1,Burlein S.2,Thomson B. R.3,Booth C. J.4,Knauf F.5,Wang T.6,Aronson P. S.16ORCID

Affiliation:

1. Department of Internal Medicine, Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut

2. Department of Nephrology and Hypertension, Friedrich Alexander Universität Erlangen-Nürnberg, Erlangen, Germany

3. Feinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, Illinois

4. Department of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut

5. Department of Nephrology and Medical Intensive Care, Charité Universitätsmedizin Berlin, Berlin, Germany

6. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut

Abstract

Ksp-cadherin (cadherin-16) is an atypical member of the cadherin superfamily of cell adhesion molecules that is ubiquitously expressed on the basolateral membrane of epithelial cells lining the nephron and the collecting system. Using knockout mice, we found that Ksp-cadherin is in fact not required for kidney development despite its high and specific expression along the nephron. However, its absence leads to a developmental delay in maximal urinary concentrating ability.

Funder

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Physiological Society

Subject

Physiology

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