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Am J Physiol Renal Physiol 294: F1238-F1248, 2008. First published March 5, 2008; doi:10.1152/ajprenal.00326.2007
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Mesenchymal transition in kidney collecting duct epithelial cells

Larissa Ivanova, Michael J. Butt, and Douglas G. Matsell

Department of Pediatrics and Child and Family Research Institute, British Columbia Children's Hospital, Vancouver, British Columbia, Canada

Submitted 14 July 2007 ; accepted in final form 28 February 2008

Progressive organ damage due to tissue scarring and fibrosis is a paradigm shared by numerous human diseases including chronic kidney disease. The purpose of this study was to confirm the hypothesis that collecting duct (CD) epithelial cells can undergo mesenchymal transition (EMT) in vitro. The mechanism by which CDs undergo EMT is complex and involves both early and late cellular events. Early events include rapid insulin-like growth factor (IGF)-induced Akt and GSK-3β phosphorylation, associated with early disruption of E-cadherin-β-catenin membrane colocalization, with translocation of E-cadherin to endosomes, with translocation of β-catenin to the nucleus, and with an increase in Snail expression. Transforming growth factor-β1, on the other hand, induced early activation of Smad3 and its translocation to the nucleus, Erk1/2 phosphorylation, and early disruption of membrane E-cadherin localization. The late consequences of these events included a phenotypic transformation of the cells to a mesenchymal morphology with associated increase in vimentin and {alpha}-smooth muscle actin protein expression and a decrease in total cellular E-cadherin expression, detectable as early as 24 h after stimulation.

epithelial-mesenchymal transition; insulin-like growth factor-I; E-cadherin


Address for reprint requests and other correspondence: D. G. Matsell, Dept. of Pediatrics, Div. of Nephrology, British Columbia Children's Hospital, K4-150, 4480 Oak St., Vancouver, BC, Canada V6H 3V4 (e-mail: dmatsell{at}cw.bc.ca)






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