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Cell Physiol Biochem. 2017;41(5):1736-1752. doi: 10.1159/000471866. Epub 2017 Mar 31.

Bone Marrow-Derived Mononuclear Cell Therapy Accelerates Renal Ischemia-Reperfusion Injury Recovery by Modulating Inflammatory, Antioxidant and Apoptotic Related Molecules.

Author information

1
Laboratory of Cellular and Molecular Physiology, Rio de Janeiro, Brazil.
2
Laboratory of Immunopathology, Rio de Janeiro, Brazil.
3
Laboratory for Clinical and Experimental Research on Vascular Biology, Biomedical Center, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
4
Confocal Microscopy Unit, Institute of Biomedical Science, Rio de Janeiro, Brazil.
5
Laboratory of Pulmonary Investigation, Institute of Biophysics Carlos Chagas Filho, Rio de Janeiro, Brazil.
6
Department of Radiology, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

BACKGROUND/AIMS:

We investigated the regenerative capacity of intravenous administration of bone marrow-derived mononuclear cells (BMMCs) in a rat model of bilateral renal ischemia/reperfusion (IR) injury and the involvement of inflammatory anti-inflammatory and other biological markers in this process.

METHODS:

Rats were subjected to 1h bilateral renal pedicle clamping. BMMCs were injected i.v 1h after reperfusion and tracked by 99mTc and GFP+ BMMCs. Twenty-four hours after reperfusion, renal function and histological changes were evaluated. The mRNA (real time PCR) and protein (ELISA and immuno-staining) expression of biological markers were analyzed.

RESULTS:

Renal function and structure improved after infusion of BMMCs in the IR group (IR-C). Labeled BMMCs were found in the kidneys after therapy. The expression of inflammatory and biological markers (TLR-2, TRL-4, RAGE, IL-17, HMGB-1, KIM-1) were reduced and the expression of anti-inflammatory and antioxidant markers (IL-10, Nrf2, and HO-1) were increased in IR-C animals compared with IR untreated animals (IR-S). The apoptotic index diminished and the proliferation index increased in IR-C compared with IR-S.

CONCLUSION:

The results contribute to our understanding of the role of different biological players in morphofunctional renal improvement and cytoprotection in a post-ischemic reperfusion kidney injury model subjected to cellular therapy.

KEYWORDS:

Bone marrow; Cellular therapy; Ischemia- reperfusion; Renal

PMID:
28365681
DOI:
10.1159/000471866
[Indexed for MEDLINE]
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