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Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury

Acute kidney injury (AKI) is a clinical condition that is associated with high morbidity and mortality. Inflammation is reported to play a key role in AKI. Although the M2 macrophages exhibit antimicrobial and anti‐inflammatory activities, their therapeutic potential has not been evaluated for AKI....

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Autores principales: Mao, Ruiwen, Wang, Chengshi, Zhang, Fuping, Zhao, Meng, Liu, Shuyun, Liao, Guangneng, Li, Lan, Chen, Younan, Cheng, Jingqiu, Liu, Jingping, Lu, Yanrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7131941/
https://www.ncbi.nlm.nih.gov/pubmed/32004417
http://dx.doi.org/10.1111/jcmm.15005
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author Mao, Ruiwen
Wang, Chengshi
Zhang, Fuping
Zhao, Meng
Liu, Shuyun
Liao, Guangneng
Li, Lan
Chen, Younan
Cheng, Jingqiu
Liu, Jingping
Lu, Yanrong
author_facet Mao, Ruiwen
Wang, Chengshi
Zhang, Fuping
Zhao, Meng
Liu, Shuyun
Liao, Guangneng
Li, Lan
Chen, Younan
Cheng, Jingqiu
Liu, Jingping
Lu, Yanrong
author_sort Mao, Ruiwen
collection PubMed
description Acute kidney injury (AKI) is a clinical condition that is associated with high morbidity and mortality. Inflammation is reported to play a key role in AKI. Although the M2 macrophages exhibit antimicrobial and anti‐inflammatory activities, their therapeutic potential has not been evaluated for AKI. This study aimed to investigate the protective effect of peritoneal M2 macrophage transplantation on AKI in mice. The macrophages were isolated from peritoneal dialysates of mice. The macrophages were induced to undergo M2 polarization using interleukin (IL)‐4/IL‐13. AKI was induced in mice by restoring the blood supply after bilateral renal artery occlusion for 30 minutes. The macrophages were injected into the renal cortex of mice. The changes in renal function, inflammation and tubular proliferation were measured. The M2 macrophages were co‐cultured with the mouse primary proximal tubular epithelial cells (PTECs) under hypoxia/reoxygenation conditions in vitro. The PTEC apoptosis and proliferation were analysed. The peritoneal M2 macrophages effectively alleviated the renal injury and inflammatory response in mice with ischaemia‐reperfusion injury (IRI) and promoted the PTEC proliferation in vivo and in vitro. These results indicated that the peritoneal M2 macrophages ameliorated AKI by decreasing inflammatory response and promoting PTEC proliferation. Hence, the peritoneal M2 macrophage transplantation can serve as a potential cell therapy for renal diseases.
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spelling pubmed-71319412020-04-06 Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury Mao, Ruiwen Wang, Chengshi Zhang, Fuping Zhao, Meng Liu, Shuyun Liao, Guangneng Li, Lan Chen, Younan Cheng, Jingqiu Liu, Jingping Lu, Yanrong J Cell Mol Med Original Articles Acute kidney injury (AKI) is a clinical condition that is associated with high morbidity and mortality. Inflammation is reported to play a key role in AKI. Although the M2 macrophages exhibit antimicrobial and anti‐inflammatory activities, their therapeutic potential has not been evaluated for AKI. This study aimed to investigate the protective effect of peritoneal M2 macrophage transplantation on AKI in mice. The macrophages were isolated from peritoneal dialysates of mice. The macrophages were induced to undergo M2 polarization using interleukin (IL)‐4/IL‐13. AKI was induced in mice by restoring the blood supply after bilateral renal artery occlusion for 30 minutes. The macrophages were injected into the renal cortex of mice. The changes in renal function, inflammation and tubular proliferation were measured. The M2 macrophages were co‐cultured with the mouse primary proximal tubular epithelial cells (PTECs) under hypoxia/reoxygenation conditions in vitro. The PTEC apoptosis and proliferation were analysed. The peritoneal M2 macrophages effectively alleviated the renal injury and inflammatory response in mice with ischaemia‐reperfusion injury (IRI) and promoted the PTEC proliferation in vivo and in vitro. These results indicated that the peritoneal M2 macrophages ameliorated AKI by decreasing inflammatory response and promoting PTEC proliferation. Hence, the peritoneal M2 macrophage transplantation can serve as a potential cell therapy for renal diseases. John Wiley and Sons Inc. 2020-01-31 2020-03 /pmc/articles/PMC7131941/ /pubmed/32004417 http://dx.doi.org/10.1111/jcmm.15005 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Mao, Ruiwen
Wang, Chengshi
Zhang, Fuping
Zhao, Meng
Liu, Shuyun
Liao, Guangneng
Li, Lan
Chen, Younan
Cheng, Jingqiu
Liu, Jingping
Lu, Yanrong
Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
title Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
title_full Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
title_fullStr Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
title_full_unstemmed Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
title_short Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
title_sort peritoneal m2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7131941/
https://www.ncbi.nlm.nih.gov/pubmed/32004417
http://dx.doi.org/10.1111/jcmm.15005
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