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Nichols LA, Grunz-Borgmann EA, Wang X, et al. A role for the age-dependent loss of α(E)-catenin in regulation of N-cadherin expression and cell migration. Physiol Rep. 2014;2(6)doi: 10.14814/phy2.12039.
Nichols, L. A., Grunz-Borgmann, E. A., Wang, X., & Parrish, A. R. (2014). A role for the age-dependent loss of α(E)-catenin in regulation of N-cadherin expression and cell migration. Physiological reports, 2(6), . https://doi.org/10.14814/phy2.12039
Nichols, LaNita A, et al. "A role for the age-dependent loss of α(E)-catenin in regulation of N-cadherin expression and cell migration." Physiological reports vol. 2,6 (2014). doi: https://doi.org/10.14814/phy2.12039
Nichols LA, Grunz-Borgmann EA, Wang X, Parrish AR. A role for the age-dependent loss of α(E)-catenin in regulation of N-cadherin expression and cell migration. Physiol Rep. 2014 Jun 11;2(6). doi: 10.14814/phy2.12039. Print 2014 Jun 01. PMID: 24920123; PMCID: PMC4208646.
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Physiol Rep. 2014 Jun 11;2(6). doi: 10.14814/phy2.12039. Print 2014 Jun 01.

A role for the age-dependent loss of α(E)-catenin in regulation of N-cadherin expression and cell migration.

Physiological reports

LaNita A Nichols, Elizabeth A Grunz-Borgmann, Xinhui Wang, Alan R Parrish

Affiliations

  1. Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, Missouri.

PMID: 24920123 PMCID: PMC4208646 DOI: 10.14814/phy2.12039

Abstract

The aging kidney has a decreased ability to repair following acute kidney injury. Previous studies from our laboratory have demonstrated a loss in α-catenin expression in the aging rat kidney. We hypothesize that loss of α-catenin expression in tubular epithelial cells may induce changes that result in a decreased repair capacity. In these studies, we demonstrate that decreased α-catenin protein expression is detectable as early as 20 months of age in male Fischer 344 rats. Protein loss is also observed in aged nonhuman primate kidneys, suggesting that this is not a species-specific response. In an effort to elucidate alterations due to the loss of α-catenin, we generated NRK-52E cell lines with stable knockdown of α(E)-catenin (C2 cells). Interestingly, C2 cells had decreased expression of N-cadherin, decreased cell-cell adhesion, and increased monolayer permeability. C2 had deficits in wound repair, due to alterations in cell migration. Analysis of gene expression in the migrating control cells indicated that expression of N-cadherin and N-CAM was increased during repair. In migrating C2 cells, expression of N-CAM was also increased, but the expression of N-cadherin was not upregulated. Importantly, a blocking antibody against N-cadherin inhibited repair in NRK-52E cells, suggesting an important role in repair. Taken together, these data suggest that loss of α-catenin, and the subsequent downregulation of N-cadherin expression, is a mechanism underlying the decreased migration of tubular epithelial cells that contributes to the inability of the aging kidney to repair following injury.

© 2014 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

Keywords: Aging; N‐cadherin; migration; wound repair; α‐catenin

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