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|Título:||Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury|
Soares, Miguel P.
Le Moine, Alain
|Palavras-chave:||Acute kidney injury|
Monocytes and macrophages
|Editora:||Nature Publishing Group|
|Citação:||Scientific Reports 7, Article number: 197 (2017) doi:10.1038/s41598-017-00220-w|
|Resumo:||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.|
|Descrição:||This work was presented in abstract form at the 17th Congress of the European Society for Organ Transplantation (ESOT) in Brussels, Belgium (Brief Oral Presentation, BOS04 – Ischemia, Reperfusion, Metabolism and Aging, abstract N°BO33; 13–16 September 2015) and at the 16th Congress of the European Association of Urology (EAU) in Munich, Germany (Poster Session 48, Kidney Transplant: From Bench to clinical practice, abstract n°603; 11–15 March 2016).|
|Versão do Editor:||http://www.nature.com/articles/s41598-017-00220-w?WT.feed_name=subjects_immunology|
|Aparece nas colecções:||I- Artigos|
Ficheiros deste registo:
|art%3A10.1038%2Fs41598-017-00220-w.pdf||artigo principal||2,19 MB||Adobe PDF||Ver/Abrir|
|41598_2017_220_MOESM1_ESM.pdf||material suplementar||2,14 MB||Adobe PDF||Ver/Abrir|
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