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Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury
Renal ischemia-reperfusion injury (IRI) is a major risk factor for delayed graft function in renal transplantation. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1) mediates protection against IRI. However, the role of myeloid HO-1 during IRI remains poorly chara...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428056/ https://www.ncbi.nlm.nih.gov/pubmed/28298633 http://dx.doi.org/10.1038/s41598-017-00220-w |
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author | Rossi, Maxime Thierry, Antoine Delbauve, Sandrine Preyat, Nicolas Soares, Miguel P. Roumeguère, Thierry Leo, Oberdan Flamand, Véronique Le Moine, Alain Hougardy, Jean-Michel |
author_facet | Rossi, Maxime Thierry, Antoine Delbauve, Sandrine Preyat, Nicolas Soares, Miguel P. Roumeguère, Thierry Leo, Oberdan Flamand, Véronique Le Moine, Alain Hougardy, Jean-Michel |
author_sort | Rossi, Maxime |
collection | PubMed |
description | Renal ischemia-reperfusion injury (IRI) is a major risk factor for delayed graft function in renal transplantation. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1) mediates protection against IRI. However, the role of myeloid HO-1 during IRI remains poorly characterized. Mice with myeloid-restricted deletion of HO-1 (HO-1(M-KO)), littermate (LT), and wild-type (WT) mice were subjected to renal IRI or sham procedures and sacrificed after 24 hours or 7 days. In comparison to LT, HO-1(M-KO) exhibited significant renal histological damage, pro-inflammatory responses and oxidative stress 24 hours after reperfusion. HO-1(M-KO) mice also displayed impaired tubular repair and increased renal fibrosis 7 days after IRI. In WT mice, HO-1 induction with hemin specifically upregulated HO-1 within the CD11b(+) F4/80(lo) subset of the renal myeloid cells. Prior administration of hemin to renal IRI was associated with significant increase of the renal HO-1(+) CD11b(+) F4/80(lo) myeloid cells in comparison to control mice. In contrast, this hemin-mediated protection was abolished in HO-1(M-KO) mice. In conclusion, myeloid HO-1 appears as a critical protective pathway against renal IRI and could be an interesting therapeutic target in renal transplantation. |
format | Online Article Text |
id | pubmed-5428056 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-54280562017-05-15 Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury Rossi, Maxime Thierry, Antoine Delbauve, Sandrine Preyat, Nicolas Soares, Miguel P. Roumeguère, Thierry Leo, Oberdan Flamand, Véronique Le Moine, Alain Hougardy, Jean-Michel Sci Rep Article Renal ischemia-reperfusion injury (IRI) is a major risk factor for delayed graft function in renal transplantation. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1) mediates protection against IRI. However, the role of myeloid HO-1 during IRI remains poorly characterized. Mice with myeloid-restricted deletion of HO-1 (HO-1(M-KO)), littermate (LT), and wild-type (WT) mice were subjected to renal IRI or sham procedures and sacrificed after 24 hours or 7 days. In comparison to LT, HO-1(M-KO) exhibited significant renal histological damage, pro-inflammatory responses and oxidative stress 24 hours after reperfusion. HO-1(M-KO) mice also displayed impaired tubular repair and increased renal fibrosis 7 days after IRI. In WT mice, HO-1 induction with hemin specifically upregulated HO-1 within the CD11b(+) F4/80(lo) subset of the renal myeloid cells. Prior administration of hemin to renal IRI was associated with significant increase of the renal HO-1(+) CD11b(+) F4/80(lo) myeloid cells in comparison to control mice. In contrast, this hemin-mediated protection was abolished in HO-1(M-KO) mice. In conclusion, myeloid HO-1 appears as a critical protective pathway against renal IRI and could be an interesting therapeutic target in renal transplantation. Nature Publishing Group UK 2017-03-15 /pmc/articles/PMC5428056/ /pubmed/28298633 http://dx.doi.org/10.1038/s41598-017-00220-w Text en © The Author(s) 2017 This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Rossi, Maxime Thierry, Antoine Delbauve, Sandrine Preyat, Nicolas Soares, Miguel P. Roumeguère, Thierry Leo, Oberdan Flamand, Véronique Le Moine, Alain Hougardy, Jean-Michel Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
title | Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
title_full | Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
title_fullStr | Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
title_full_unstemmed | Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
title_short | Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
title_sort | specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428056/ https://www.ncbi.nlm.nih.gov/pubmed/28298633 http://dx.doi.org/10.1038/s41598-017-00220-w |
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