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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 212819, 7 pages
Research Article

Explanting Is an Ex Vivo Model of Renal Epithelial-Mesenchymal Transition

1Department of Nephrology, The Royal Melbourne Hospital, Melbourne, VIC 3050, Australia
2School of Medical Sciences, RMIT University, Melbourne, VIC 3083, Australia
3Department of Medicine, The University of Melbourne, Melbourne, VIC 3010, Australia

Received 23 June 2011; Revised 1 September 2011; Accepted 1 September 2011

Academic Editor: Nick Di Girolamo

Copyright © 2011 Catherine E. Winbanks 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.


Recognised by their de novo expression of alpha-smooth muscle actin (SMA), recruitment of myofibroblasts is key to the pathogenesis of fibrosis in chronic kidney disease. Increasingly, we realise that epithelial-mesenchymal transition (EMT) may be an important source of these cells. In this study we describe a novel model of renal EMT. Rat kidney explants were finely diced on gelatin-coated Petri dishes and cultured in serum-supplemented media. Morphology and immunocytochemistry were used to identify mesenchymal (vimentin+, α-smooth muscle actin (SMA)+, desmin+), epithelial (cytokeratin+), and endothelial (RECA+) cells at various time points. Cell outgrowths were all epithelial in origin (cytokeratin+) at day 3. By day 10, 50 ± 12% (mean ± SE) of cytokeratin+ cells double-labelled for SMA, indicating EMT. Lectin staining established a proximal tubule origin. By day 17, cultures consisted only of myofibroblasts (SMA+/cytokeratin−). Explanting is a reproducible ex vivo model of EMT. The ability to modify this change in phenotype provides a useful tool to study the regulation and mechanisms of renal tubulointerstitial fibrosis.