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Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury
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 (n = 4) were sacrificed every two hours during the first...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896652/ https://www.ncbi.nlm.nih.gov/pubmed/20617137 http://dx.doi.org/10.1155/2010/193259 |
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author | Vansthertem, David Gossiaux, Annabel Declèves, Anne-Emilie Caron, Nathalie Nonclercq, Denis Legrand, Alexandre Toubeau, Gérard |
author_facet | Vansthertem, David Gossiaux, Annabel Declèves, Anne-Emilie Caron, Nathalie Nonclercq, Denis Legrand, Alexandre Toubeau, Gérard |
author_sort | Vansthertem, David |
collection | PubMed |
description | 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 (n = 4) 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-2′-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 α-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. |
format | Text |
id | pubmed-2896652 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-28966522010-07-08 Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury Vansthertem, David Gossiaux, Annabel Declèves, Anne-Emilie Caron, Nathalie Nonclercq, Denis Legrand, Alexandre Toubeau, Gérard J Biomed Biotechnol Research Article 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 (n = 4) 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-2′-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 α-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. Hindawi Publishing Corporation 2010 2010-06-14 /pmc/articles/PMC2896652/ /pubmed/20617137 http://dx.doi.org/10.1155/2010/193259 Text en 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. |
spellingShingle | Research Article Vansthertem, David Gossiaux, Annabel Declèves, Anne-Emilie Caron, Nathalie Nonclercq, Denis Legrand, Alexandre Toubeau, Gérard Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury |
title | Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury |
title_full | Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury |
title_fullStr | Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury |
title_full_unstemmed | Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury |
title_short | Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury |
title_sort | expression of nestin, vimentin, and ncam by renal interstitial cells after ischemic tubular injury |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896652/ https://www.ncbi.nlm.nih.gov/pubmed/20617137 http://dx.doi.org/10.1155/2010/193259 |
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