p53-Mediated Oxidative Stress and Tubular Injury in Rats with Glycerol-Induced Acute Kidney Injury

dc.creatorHomsi, E
dc.creatorda Silva, SM
dc.creatorde Brito, SM
dc.creatorPeixoto, EBI
dc.creatorde Faria, JBL
dc.creatorJanino, P
dc.date2011
dc.date2014-07-30T14:30:32Z
dc.date2015-11-26T17:28:30Z
dc.date2014-07-30T14:30:32Z
dc.date2015-11-26T17:28:30Z
dc.date.accessioned2018-03-29T00:15:38Z
dc.date.available2018-03-29T00:15:38Z
dc.identifierAmerican Journal Of Nephrology. Karger, v. 33, n. 1, n. 49, n. 59, 2011.
dc.identifier0250-8095
dc.identifierWOS:000286570300007
dc.identifier10.1159/000322836
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/58974
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/58974
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1285071
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionBackground/Aims: p53 is a transcriptional factor that responds to severe cell damage promoting the transcription of proapoptotic and prooxidant genes. In this study, we evaluated the role of p53 activation in glycerol-induced acute kidney injury (Gly-AKI). Methods: Rats were treated with p53 inhibitor (pifithrin-alpha) in the moment we injected glycerol. Renal function, renal histology (HE), TUNEL labeling, cleaved caspase-3 staining, renal p53, Bax, PUMA, Bcl-2, p21 and survivin expressions, renal lipid and DNA oxidative markers, and the expression of antioxidant enzymes (Mn-SOD, HO-1, and NAD(P)H:quinone-oxidoreductase-1) were evaluated. Results: Gly-AKI rats showed an increased renal expression of phosphorylated-p53. The p53 inhibitor attenuated renal impairment and significantly reduced tubular injury. The expression of the oxidative markers was significantly reduced in treated rats. Proapoptotic and prooxidant proteins Bax and PUMA were overexpressed in Gly-AKI rats and reduced in treated rats. On the contrary, antiapoptotic Bcl-2, p21, and survivin showed a tendency to increase in treated rats. The antioxidant enzymes' expression remained elevated or in-creased in treated rats. Conclusion: On the whole, p53 inhibition was protective in the short term. The oxidative stress subsided and the transcription tipped toward prosurvival genes; consequently tubular injury was attenuated in treated rats. Copyright (C) 2010 S. Karger AG, Basel
dc.description33
dc.description1
dc.description49
dc.description59
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionSao Paulo, Brazil
dc.descriptionFAEP/FUNCAMP, Campinas, Brazil
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageen
dc.publisherKarger
dc.publisherBasel
dc.publisherSuíça
dc.relationAmerican Journal Of Nephrology
dc.relationAm. J. Nephrol.
dc.rightsfechado
dc.rightshttp://www.karger.com/Services/RightsPermissions
dc.sourceWeb of Science
dc.subjectAcute kidney injury
dc.subjectOxidative stress
dc.subjectTranscriptional factor
dc.subjectApoptosis
dc.subjectp53
dc.subjectAcute-renal-failure
dc.subjectTumor-suppressor
dc.subjectP53 Inhibitor
dc.subjectCell-death
dc.subjectApoptosis
dc.subjectTranscription
dc.subjectMitochondria
dc.subjectMyoglobin
dc.subjectSurvivin
dc.subjectGene
dc.titlep53-Mediated Oxidative Stress and Tubular Injury in Rats with Glycerol-Induced Acute Kidney Injury
dc.typeArtículos de revistas


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