RGD Reference Report - Mesenchymal stem cell therapy prevents interstitial fibrosis and tubular atrophy in a rat kidney allograft model. - Rat Genome Database

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Mesenchymal stem cell therapy prevents interstitial fibrosis and tubular atrophy in a rat kidney allograft model.

Authors: Franquesa, M  Herrero, E  Torras, J  Ripoll, E  Flaquer, M  Goma, M  Lloberas, N  Anegon, I  Cruzado, JM  Grinyo, JM  Herrero-Fresneda, I 
Citation: Franquesa M, etal., Stem Cells Dev. 2012 Nov 20;21(17):3125-35. doi: 10.1089/scd.2012.0096. Epub 2012 May 18.
RGD ID: 9068431
Pubmed: PMID:22494435   (View Abstract at PubMed)
PMCID: PMC3495114   (View Article at PubMed Central)
DOI: DOI:10.1089/scd.2012.0096   (Journal Full-text)

In solid organ transplantation, mesenchymal stem cell (MSC) therapy is strongly emerging among other cell therapies due to the positive results obtained in vitro and in vivo as an immunomodulatory agent and their potential regenerative role. We aimed at testing whether a single dose of MSCs, injected at 11 weeks after kidney transplantation for the prevention of chronic mechanisms, enhanced regeneration and provided protection against the inflammatory and fibrotic processes that finally lead to the characteristic features of chronic allograft nephropathy (CAN). Either bone marrow mononuclear cells (BMCs) injection or no-therapy (NT) were used as control treatments. A rat kidney transplantation model of CAN with 2.5 h of cold ischemia was used, and functional, histological, and molecular parameters were assessed at 12 and 24 weeks after transplantation. MSC and BMC cell therapy preserves renal function at 24 weeks and abrogates proteinuria, which is typical of this model (NT24w: 68.9 +/- 26.5 mg/24 h, MSC24w: 16.6 +/- 2.3 mg/24 h, BMC24w: 24.1 +/- 5.3 mg/24 h, P<0.03). Only MSC-treated animals showed a reduction in interstitial fibrosis and tubular atrophy (NT24w: 2.3 +/- 0.29, MSC24w: 0.4 +/- 0.2, P<0.03), less T cells (NT: 39.6 +/- 9.5, MSC: 8.1 +/- 0.9, P<0.03) and macrophages (NT: 20.9 +/- 4.7, MSC: 5.9 +/- 1.7, P<0.05) infiltrating the parenchyma and lowered expression of inflammatory cytokines while increasing the expression of anti-inflammatory factors. MSCs appear to serve as a protection from injury development rather than regenerate the damaged tissue, as no differences were observed in Ki67 expression, and kidney injury molecule-1, Clusterin, NGAL, and hepatocyte growth factor expression were only up-regulated in nontreated animals. Considering the results, a single delayed MSC injection is effective for the long-term protection of kidney allografts.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Chronic Allograft Nephropathy treatmentISOClu (Rattus norvegicus)9068431; 9068431 RGD 
Chronic Allograft Nephropathy treatmentIEP 9068431 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Clu  (clusterin)

Genes (Mus musculus)
Clu  (clusterin)

Genes (Homo sapiens)
CLU  (clusterin)


Additional Information