Troglitazone Induces Extracellular Matrix and Cytoskeleton Remodeling in Mouse Collecting Duct CellsReport as inadecuate

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Journal of Biomedicine and BiotechnologyVolume 2012 2012, Article ID 507057, 10 pages

Research Article Department of Cellular and Molecular Medicine, Kidney Research Centre, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada K1H 8M5

Received 16 September 2011; Revised 9 November 2011; Accepted 15 November 2011

Academic Editor: Beric Henderson

Copyright © 2012 Jaime Corinaldi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Peroxisome proliferator-activated receptor PPARγ has been shown to have a protective role in the nephron through its ability to inhibit a transforming growth factor- TGF-β mediated fibrotic response. In contrast, PPARγ was also shown to induce a mesenchymal transformation in epithelial intestinal cells. A fibrotic response in the collecting duct has only recently been established; however, the entire collecting duct has not been fully examined. Inner medullary collecting duct cells IMCD-K2 and mouse cortical collecting duct cells M1, representing the cortical and medullary collecting duct, were exposed to 5–10 μM troglitazone for 24 hours. Troglitazone resulted in an elongated morphology, 60% decreases in E-cadherin and β-catenin, a 35% decrease in α-catenin, and a 1.5-fold increase in fibronectin. These effects were not reversed with PPARγ antagonists or affected with PPARγ overexpression. Our results indicate that troglitazone induced a mesenchymal-like transformation in M1 and IMCD-K2 epithelial cells independently of PPARγ.

Author: Jaime Corinaldi, Rania Nasrallah, Jordan Clark, Geneviève Paris, Pedro Miura, Bernard J. Jasmin, and Richard L. Hébert



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