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Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury

Low‐energy shock wave (LESW) has been recognized as a promising non‐invasive intervention to prevent the organs or tissues against ischaemia reperfusion injury (IRI), whereas its effect on kidney injury is rarely explored. To investigate the protective role of pretreatment with LESW on renal IRI in...

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Autores principales: Liu, Jingyu, Dou, Quanliang, Zhou, Changcheng, Zhou, Liuhua, Zhao, Feng, Xu, Luwei, Xu, Zheng, Ge, Yuzheng, Wu, Ran, Jia, Ruipeng
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/PMC7521246/
https://www.ncbi.nlm.nih.gov/pubmed/32761803
http://dx.doi.org/10.1111/jcmm.15678
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author Liu, Jingyu
Dou, Quanliang
Zhou, Changcheng
Zhou, Liuhua
Zhao, Feng
Xu, Luwei
Xu, Zheng
Ge, Yuzheng
Wu, Ran
Jia, Ruipeng
author_facet Liu, Jingyu
Dou, Quanliang
Zhou, Changcheng
Zhou, Liuhua
Zhao, Feng
Xu, Luwei
Xu, Zheng
Ge, Yuzheng
Wu, Ran
Jia, Ruipeng
author_sort Liu, Jingyu
collection PubMed
description Low‐energy shock wave (LESW) has been recognized as a promising non‐invasive intervention to prevent the organs or tissues against ischaemia reperfusion injury (IRI), whereas its effect on kidney injury is rarely explored. To investigate the protective role of pretreatment with LESW on renal IRI in rats, animals were randomly divided into Sham, LESW, IRI and LESW + IRI groups. At 4, 12, 24 hours and 3 and 7 days after reperfusion, serum samples and renal tissues were harvested for performing the analysis of renal function, histopathology, immunohistochemistry, flow cytometry and Western blot, as well as enzyme‐linked immunosorbent assay. Moreover, circulating endothelial progenitor cells (EPCs) were isolated, labelled with fluorescent dye and injected by tail vein. The fluorescent signals of EPCs were detected using fluorescence microscope and in vivo imaging system to track the distribution of injected circulating EPCs. Results showed that pretreatment with LESW could significantly reduce kidney injury biomarkers, tubular damage, and cell apoptosis, and promote cell proliferation and vascularization in IRI kidneys. The renoprotective role of LESW pretreatment would be attributed to the remarkably increased EPCs in the treated kidneys, part of which were recruited from circulation through SDF‐1/CXCR7 pathway. In conclusion, pretreatment with LESW could increase the recruitment of circulating EPCs to attenuate and repair renal IRI.
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spelling pubmed-75212462020-09-30 Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury Liu, Jingyu Dou, Quanliang Zhou, Changcheng Zhou, Liuhua Zhao, Feng Xu, Luwei Xu, Zheng Ge, Yuzheng Wu, Ran Jia, Ruipeng J Cell Mol Med Original Articles Low‐energy shock wave (LESW) has been recognized as a promising non‐invasive intervention to prevent the organs or tissues against ischaemia reperfusion injury (IRI), whereas its effect on kidney injury is rarely explored. To investigate the protective role of pretreatment with LESW on renal IRI in rats, animals were randomly divided into Sham, LESW, IRI and LESW + IRI groups. At 4, 12, 24 hours and 3 and 7 days after reperfusion, serum samples and renal tissues were harvested for performing the analysis of renal function, histopathology, immunohistochemistry, flow cytometry and Western blot, as well as enzyme‐linked immunosorbent assay. Moreover, circulating endothelial progenitor cells (EPCs) were isolated, labelled with fluorescent dye and injected by tail vein. The fluorescent signals of EPCs were detected using fluorescence microscope and in vivo imaging system to track the distribution of injected circulating EPCs. Results showed that pretreatment with LESW could significantly reduce kidney injury biomarkers, tubular damage, and cell apoptosis, and promote cell proliferation and vascularization in IRI kidneys. The renoprotective role of LESW pretreatment would be attributed to the remarkably increased EPCs in the treated kidneys, part of which were recruited from circulation through SDF‐1/CXCR7 pathway. In conclusion, pretreatment with LESW could increase the recruitment of circulating EPCs to attenuate and repair renal IRI. John Wiley and Sons Inc. 2020-08-06 2020-09 /pmc/articles/PMC7521246/ /pubmed/32761803 http://dx.doi.org/10.1111/jcmm.15678 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
Liu, Jingyu
Dou, Quanliang
Zhou, Changcheng
Zhou, Liuhua
Zhao, Feng
Xu, Luwei
Xu, Zheng
Ge, Yuzheng
Wu, Ran
Jia, Ruipeng
Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
title Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
title_full Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
title_fullStr Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
title_full_unstemmed Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
title_short Low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
title_sort low‐energy shock wave pretreatment recruit circulating endothelial progenitor cells to attenuate renal ischaemia reperfusion injury
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521246/
https://www.ncbi.nlm.nih.gov/pubmed/32761803
http://dx.doi.org/10.1111/jcmm.15678
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