The role of heme oxygenase 1 in rapamycin-induced renal dysfunction after ischemia and reperfusion injury

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dc.contributor.authorGoncalves, G. M.
dc.contributor.authorCenedeze, Marcos Antonio [UNIFESP]
dc.contributor.authorFeitoza, C. Q.
dc.contributor.authorWang, P. M. H.
dc.contributor.authorBertocchi, A. P. F.
dc.contributor.authorDamiao, M. J.
dc.contributor.authorPinheiro, H. S.
dc.contributor.authorTeixeira, V. P. Antunes
dc.contributor.authorReis, M. A. dos
dc.contributor.authorPacheco-Silva, A.
dc.contributor.authorCamara, N. O. S.
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Fed Triangulo Mineiro
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2016-01-24T12:41:32Z
dc.date.available2016-01-24T12:41:32Z
dc.date.issued2006-11-01
dc.description.abstractIschemia and reperfusion injury ( IRI) is the main etiology of acute renal failure in native and transplanted kidneys. in the transplantation field, immunosuppressive drugs may play an additional role in acute graft dysfunction. Rapamycin may impair renal regeneration post IRI. Heme oxygenase 1 ( HO-1) is a protective gene with anti-inflammatory and anti-apoptotic actions. We investigated whether HO-1 played a role in rapamycin-induced renal dysfunction in an established model of IRI. Rapamycin ( 3mg/kg) was administered to mice before being subjected to 45 min of ischemia. Animals subjected to IRI presented with impaired renal function that peaked at 24h ( 2.05 +/- 0.23mg/dl), decreasing thereafter. Treatment with rapamycin caused even more renal dysfunctions ( 2.30 +/- 0.33mg/dl), sustained up to 120 h after reperfusion ( 1.54 +/- 0.4mg/dl), when compared to the control ( 0.63 +/- 0.09mg/dl, P < 0.05). Rapamycin delayed tubular regeneration that was normally higher in the control group at day 5 ( 68.53 +/- 2.30 vs 43.63 +/- 3.11%, P < 0.05). HO-1 was markedly upregulated after IRI and its expression was even enhanced by rapamycin ( 1.32-fold). However, prior induction of HO-1 by cobalt protoporphyrin improved the renal dysfunction imposed by rapamycin, mostly at later time points. These results demonstrated that rapamycin used in ischemic-injured organs could also negatively affect post-transplantation recovery. Modulation of HO-1 expression may represent a feasible approach to limit rapamycin acute toxicity.en
dc.description.affiliationUniversidade Federal de São Paulo, Disciplina Nefrol, Escola Paulista Med, Div Nephrol,Lab Imunol Clin & Expt, BR-04023900 São Paulo, Brazil
dc.description.affiliationUniv Fed Triangulo Mineiro, Dept Pathol, Uberaba, MG, Brazil
dc.description.affiliationUniv São Paulo, Dept Immunol, Lab Imunol Transplantes, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Disciplina Nefrol, Escola Paulista Med, Div Nephrol,Lab Imunol Clin & Expt, BR-04023900 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent1742-1749
dc.identifierhttp://dx.doi.org/10.1038/sj.ki.5001893
dc.identifier.citationKidney International. New York: Nature Publishing Group, v. 70, n. 10, p. 1742-1749, 2006.
dc.identifier.doi10.1038/sj.ki.5001893
dc.identifier.issn0085-2538
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29212
dc.identifier.wosWOS:000241936500014
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofKidney International
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectischemia and reperfusion injuryen
dc.subjectrapamycinen
dc.subjectheme oxygenase 1en
dc.titleThe role of heme oxygenase 1 in rapamycin-induced renal dysfunction after ischemia and reperfusion injuryen
dc.typeinfo:eu-repo/semantics/article
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