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Wnt/脽-catenin pathway in podocytes integrates cell adhesion, differentiation,
and survival.
Authors Kato H, Gruenwald A, Suh JH, Miner JH, Barisoni-Thomas L, Taketo MM, Faul C,
Millar SE, Holzman LB, Susztak K
Submitted By Lawrence Holzman on 12/10/2012
Status Published
Journal The Journal of biological chemistry
Year 2011
Date Published 7/22/2011
Volume : Pages 286 : 26003 - 26015
PubMed Reference
Abstract Diabetic kidney disease (DKD) is the single most common cause of albuminuria and
end-stage kidney disease in the United States. We found increased expression of
Wnt/脽-catenin (Ctnnb1) pathway transcripts and proteins in glomeruli and
podocytes of patients and mouse models of DKD. Mice with podocyte-specific
expression of stabilized Ctnnb1 exhibited basement membrane abnormalities,
albuminuria, and increased susceptibility to glomerular injury. Mice with
podocyte-specific deletion of Ctnnb1 or podocyte-specific expression of the
canonical Wnt inhibitor Dickkopf-related protein 1 (Dkk1) also showed increased
susceptibility to DKD. Podocytes with stabilized Ctnnb1 were less motile and
less adhesive to different matrices. Deletion of Ctnnb1 in cultured podocytes
increased the expression of podocyte differentiation markers and enhanced cell
motility; however, these cells were more susceptible to apoptosis. These results
indicate that Wnt/Ctnnb1 signaling in podocytes plays a critical role in
integrating cell adhesion, motility, cell death, and differentiation. Balanced
Ctnnb1 expression is critical for glomerular filtration barrier maintenance.


Investigators with authorship
NameInstitution
Lawrence HolzmanUniversity of Pennsylvania

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