Unknown

Dataset Information

0

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 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.

SUBMITTER: Rossi M 

PROVIDER: S-EPMC5428056 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

altmetric image

Publications

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

Rossi Maxime M   Thierry Antoine A   Delbauve Sandrine S   Preyat Nicolas N   Soares Miguel P MP   Roumeguère Thierry T   Leo Oberdan O   Flamand Véronique V   Le Moine Alain A   Hougardy Jean-Michel JM  

Scientific reports 20170315 1


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<sup>M-KO</sup>), littermate (LT), and wild-type (WT) mice were subjected to renal IRI or sham procedures and sacrificed after 24 hours or  ...[more]

Similar Datasets

| S-EPMC2956932 | biostudies-literature
| S-EPMC3012573 | biostudies-literature
| S-EPMC5560494 | biostudies-other
| S-EPMC5884687 | biostudies-literature
| S-EPMC6933315 | biostudies-literature
| S-EPMC6237471 | biostudies-literature
| S-EPMC10570260 | biostudies-literature
| S-EPMC3769390 | biostudies-literature
| S-EPMC5958683 | biostudies-literature
| S-EPMC4636952 | biostudies-literature