Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury

Abstract 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 poo...

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Autores principales:	Maxime Rossi, Antoine Thierry, Sandrine Delbauve, Nicolas Preyat, Miguel P. Soares, Thierry Roumeguère, Oberdan Leo, Véronique Flamand, Alain Le Moine, Jean-Michel Hougardy
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/527ac6c697954f86bb929297f1a96352
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spelling	oai:doaj.org-article:527ac6c697954f86bb929297f1a963522021-12-02T16:08:00ZSpecific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury10.1038/s41598-017-00220-w2045-2322https://doaj.org/article/527ac6c697954f86bb929297f1a963522017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00220-whttps://doaj.org/toc/2045-2322Abstract 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-1M-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-1M-KO exhibited significant renal histological damage, pro-inflammatory responses and oxidative stress 24 hours after reperfusion. HO-1M-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+ F4/80lo subset of the renal myeloid cells. Prior administration of hemin to renal IRI was associated with significant increase of the renal HO-1+ CD11b+ F4/80lo myeloid cells in comparison to control mice. In contrast, this hemin-mediated protection was abolished in HO-1M-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.Maxime RossiAntoine ThierrySandrine DelbauveNicolas PreyatMiguel P. SoaresThierry RoumeguèreOberdan LeoVéronique FlamandAlain Le MoineJean-Michel HougardyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Maxime Rossi Antoine Thierry Sandrine Delbauve Nicolas Preyat Miguel P. Soares Thierry Roumeguère Oberdan Leo Véronique Flamand Alain Le Moine Jean-Michel Hougardy Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury
description	Abstract 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-1M-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-1M-KO exhibited significant renal histological damage, pro-inflammatory responses and oxidative stress 24 hours after reperfusion. HO-1M-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+ F4/80lo subset of the renal myeloid cells. Prior administration of hemin to renal IRI was associated with significant increase of the renal HO-1+ CD11b+ F4/80lo myeloid cells in comparison to control mice. In contrast, this hemin-mediated protection was abolished in HO-1M-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	article
author	Maxime Rossi Antoine Thierry Sandrine Delbauve Nicolas Preyat Miguel P. Soares Thierry Roumeguère Oberdan Leo Véronique Flamand Alain Le Moine Jean-Michel Hougardy
author_facet	Maxime Rossi Antoine Thierry Sandrine Delbauve Nicolas Preyat Miguel P. Soares Thierry Roumeguère Oberdan Leo Véronique Flamand Alain Le Moine Jean-Michel Hougardy
author_sort	Maxime Rossi
title	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_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_sort	specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/527ac6c697954f86bb929297f1a96352
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Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury

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