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Specific Expression of Heme Oxygenase-1 by Myeloid Cells Modulates Renal Ischemia-reperfusion Injury

Overview
Journal Sci Rep
Specialty Science
Date 2017 Mar 17
PMID 28298633
Citations 26
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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-1), 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 exhibited significant renal histological damage, pro-inflammatory responses and oxidative stress 24 hours after reperfusion. HO-1 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 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 myeloid cells in comparison to control mice. In contrast, this hemin-mediated protection was abolished in HO-1 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.

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References
1.
Correa-Costa M, Azevedo H, Amano M, Goncalves G, Hyane M, Cenedeze M . Transcriptome analysis of renal ischemia/reperfusion injury and its modulation by ischemic pre-conditioning or hemin treatment. PLoS One. 2012; 7(11):e49569. PMC: 3498198. DOI: 10.1371/journal.pone.0049569. View

2.
Lin S, Li B, Rao S, Yeo E, Hudson T, Nowlin B . Macrophage Wnt7b is critical for kidney repair and regeneration. Proc Natl Acad Sci U S A. 2010; 107(9):4194-9. PMC: 2840080. DOI: 10.1073/pnas.0912228107. View

3.
de Wilde V, Van Rompaey N, Hill M, Lebrun J, Lemaitre P, Lhomme F . Endotoxin-induced myeloid-derived suppressor cells inhibit alloimmune responses via heme oxygenase-1. Am J Transplant. 2009; 9(9):2034-47. DOI: 10.1111/j.1600-6143.2009.02757.x. View

4.
Kie J, Kapturczak M, Traylor A, Agarwal A, Hill-Kapturczak N . Heme oxygenase-1 deficiency promotes epithelial-mesenchymal transition and renal fibrosis. J Am Soc Nephrol. 2008; 19(9):1681-91. PMC: 2518436. DOI: 10.1681/ASN.2007101099. View

5.
Lee S, Huen S, Nishio H, Nishio S, Lee H, Choi B . Distinct macrophage phenotypes contribute to kidney injury and repair. J Am Soc Nephrol. 2011; 22(2):317-26. PMC: 3029904. DOI: 10.1681/ASN.2009060615. View