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Journal of Biomedicine and Biotechnology
Volume 2010, Article ID 193259, 10 pages
Research Article

Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury

1Laboratory of Histology, Faculty of Medicine and Pharmacy, University of Mons, Avenue du Champ de Mars, 6 (Pentagone) 1B, 7000 Mons, Belgium
2Laboratory of Physiology and Pharmacology, Faculty of Medicine and Pharmacy, University of Mons, 7000 Mons, Belgium
3Laboratory of General Physiology, Faculty of Medicine, Facultés Universitaires Notre-Dame de la Paix, 5000 Namur, Belgium

Received 1 December 2009; Revised 12 March 2010; Accepted 13 April 2010

Academic Editor: Anton M. Jetten

Copyright © 2010 David Vansthertem 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.


This work explores the distribution of various markers expressed by interstitial cells in rat kidneys after ischemic injury (35 minutes) during regeneration of S3 tubules of outer stripe of outer medulla (OSOM). Groups of experimental animals ( ) were sacrificed every two hours during the first 24 hours post-ischemia as well as 2, 3, 7, 14 days post-ischemia. The occurrence of lineage markers was analyzed on kidney sections by immunohistochemistry and morphometry during the process of tubular regeneration. In postischemic kidneys, interstitial cell proliferation, assessed by 5-bromo- -deoxyuridine (BrdU) and Proliferating Cell Nuclear Antigen (PCNA) labeling, was prominent in outer medulla and reach a maximum between 24 and 72 hours after reperfusion. This population was characterized by the coexpression of vimentin and nestin. The density of -Neural Cell Adhesion Molecule (NCAM) positive interstitial cells increased transiently (18–72 hours) in the vicinity of altered tubules. We have also localized a small population of -Smooth Muscle Actin (SMA)-positive cells confined to chronically altered areas and characterized by a small proliferative index. In conclusion, we observed in the postischemic kidney a marked proliferation of interstitial cells that underwent transient phenotypical modifications. These interstitial cells could be implicated in processes leading to renal fibrosis.