Renal telocytes contribute to the repair of ischemically injured renal tubules

Telocytes (TCs), a distinct type of interstitial cells, have been identified in many organs via electron microscopy. However, their precise function in organ regeneration remains unknown. This study investigated the paracrine effect of renal TCs on renal tubular epithelial cells (TECs) in vitro, the...

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Main Authors: Li, Liping, Lin, Miao, Li, Long, Wang, Rulin, Zhang, Chao, Qi, Guisheng, Xu, Ming, Rong, Ruiming, Zhu, Tongyu
Format: Online
Language:English
Published: John Wiley & Sons, Ltd 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508154/
id pubmed-4508154
recordtype oai_dc
spelling pubmed-45081542015-07-22 Renal telocytes contribute to the repair of ischemically injured renal tubules Li, Liping Lin, Miao Li, Long Wang, Rulin Zhang, Chao Qi, Guisheng Xu, Ming Rong, Ruiming Zhu, Tongyu Original Articles Telocytes (TCs), a distinct type of interstitial cells, have been identified in many organs via electron microscopy. However, their precise function in organ regeneration remains unknown. This study investigated the paracrine effect of renal TCs on renal tubular epithelial cells (TECs) in vitro, the regenerative function of renal TCs in renal tubules after ischaemia–reperfusion injury (IRI) in vivo and the possible mechanisms involved. In a renal IRI model, transplantation of renal TCs was found to decrease serum creatinine and blood urea nitrogen (BUN) levels, while renal fibroblasts exerted no such effect. The results of histological injury assessments and the expression levels of cleaved caspase-3 were consistent with a change in kidney function. Our data suggest that the protective effect of TCs against IRI occurs via inflammation-independent mechanisms in vivo. Furthermore, we found that renal TCs could not directly promote the proliferation and anti-apoptosis properties of TECs in vitro. TCs did not display any advantage in paracrine growth factor secretion in vitro compared with renal fibroblasts. These data indicate that renal TCs protect against renal IRI via an inflammation-independent pathway and that growth factors play a significant role in this mechanism. Renal TCs may protect TECs in certain microenvironments while interacting with other cells. John Wiley & Sons, Ltd 2014-06 2014-04-24 /pmc/articles/PMC4508154/ /pubmed/24758589 http://dx.doi.org/10.1111/jcmm.12274 Text en © 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. http://creativecommons.org/licenses/by/3.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Li, Liping
Lin, Miao
Li, Long
Wang, Rulin
Zhang, Chao
Qi, Guisheng
Xu, Ming
Rong, Ruiming
Zhu, Tongyu
spellingShingle Li, Liping
Lin, Miao
Li, Long
Wang, Rulin
Zhang, Chao
Qi, Guisheng
Xu, Ming
Rong, Ruiming
Zhu, Tongyu
Renal telocytes contribute to the repair of ischemically injured renal tubules
author_facet Li, Liping
Lin, Miao
Li, Long
Wang, Rulin
Zhang, Chao
Qi, Guisheng
Xu, Ming
Rong, Ruiming
Zhu, Tongyu
author_sort Li, Liping
title Renal telocytes contribute to the repair of ischemically injured renal tubules
title_short Renal telocytes contribute to the repair of ischemically injured renal tubules
title_full Renal telocytes contribute to the repair of ischemically injured renal tubules
title_fullStr Renal telocytes contribute to the repair of ischemically injured renal tubules
title_full_unstemmed Renal telocytes contribute to the repair of ischemically injured renal tubules
title_sort renal telocytes contribute to the repair of ischemically injured renal tubules
description Telocytes (TCs), a distinct type of interstitial cells, have been identified in many organs via electron microscopy. However, their precise function in organ regeneration remains unknown. This study investigated the paracrine effect of renal TCs on renal tubular epithelial cells (TECs) in vitro, the regenerative function of renal TCs in renal tubules after ischaemia–reperfusion injury (IRI) in vivo and the possible mechanisms involved. In a renal IRI model, transplantation of renal TCs was found to decrease serum creatinine and blood urea nitrogen (BUN) levels, while renal fibroblasts exerted no such effect. The results of histological injury assessments and the expression levels of cleaved caspase-3 were consistent with a change in kidney function. Our data suggest that the protective effect of TCs against IRI occurs via inflammation-independent mechanisms in vivo. Furthermore, we found that renal TCs could not directly promote the proliferation and anti-apoptosis properties of TECs in vitro. TCs did not display any advantage in paracrine growth factor secretion in vitro compared with renal fibroblasts. These data indicate that renal TCs protect against renal IRI via an inflammation-independent pathway and that growth factors play a significant role in this mechanism. Renal TCs may protect TECs in certain microenvironments while interacting with other cells.
publisher John Wiley & Sons, Ltd
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508154/
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