Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348882
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampHomsi, Eduardo-
dc.typeArtigopt_BR
dc.titleEndogenous hepatocyte growth factor attenuates inflammatory response in glycerol-induced acute kidney injurypt_BR
dc.contributor.authorHomsi, E-
dc.contributor.authorJanino, P-
dc.contributor.authorAmano, M.-
dc.contributor.authorSaraiva Camara, N.O-
dc.subjectHepatócitospt_BR
dc.subjectGlicerolpt_BR
dc.subject.otherlanguageHepatocytespt_BR
dc.subject.otherlanguageGlycerolpt_BR
dc.description.abstractHepatocyte growth factor (HGF) is overexpressed after acute kidney injury (AKI). The aim of this study was to evaluate the role of endogenous HGF in the progression of the inflammatory response in glycerol-induced AKI (Gly-AKI) in rats. Methods: Renal and systemic HGF expressions were evaluated during the development of Gly-AKI. Subsequently, the blockade of endogenous HGF was analyzed in rats treated with anti-HGF antibody concomitant to glycerol injection. Apoptosis, cell infiltration and chemokine and cytokine profiles were investigated. Results: We detected an early peak of renal and plasma HGF protein expressions 3 h after glycerol injection. The pharmacological blockade of the endogenous HGF exacerbated the renal impairment, the tubular apoptosis, the renal expression of monocyte chemoattractant protein-1 and the macrophage, CD43+, CD4+ and CD8+ T lymphocytes renal infiltration. The analysis of mRNA expressions of Th1 (t-bet, TNF-α, IL-1β) and Th2 (gata-3, IL-4, IL-10) cytokines showed a Th1-polarized response in Gly-AKI rats that was aggravated with the anti-HGF treatment. Conclusion: Endogenous HGF attenuates the renal inflammatory response, leukocyte infiltration and Th1 polarization after glycerol injection. The control of cellular immune response may partly explain the protective effect of endogenous HGF in the development of Gly-AKIpt_BR
dc.relation.ispartofAmerican journal of nephrologypt_BR
dc.relation.ispartofabbreviationAm. j. nephrol.pt_BR
dc.publisher.cityBaselpt_BR
dc.publisher.countrySuiçapt_BR
dc.publisherS. Kargerpt_BR
dc.date.issued2009-
dc.date.monthofcirculationMar.pt_BR
dc.language.isoengpt_BR
dc.description.volume29pt_BR
dc.description.issuenumber4pt_BR
dc.description.firstpage283pt_BR
dc.description.lastpage291pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0250-8095pt_BR
dc.identifier.eissn1421-9670pt_BR
dc.identifier.doi10.1159/000159275pt_BR
dc.identifier.urlhttps://www.karger.com/Article/FullText/159275pt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumberNão tempt_BR
dc.date.available2020-09-08T19:12:38Z-
dc.date.accessioned2020-09-08T19:12:38Z-
dc.description.provenanceSubmitted by Susilene Barbosa da Silva (susilene@unicamp.br) on 2020-09-08T19:12:38Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:12:56Z : No. of bitstreams: 1 000261132100001.pdf: 1236655 bytes, checksum: 17beb01df9874095f916d43584ab23d3 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-08T19:12:38Z (GMT). No. of bitstreams: 0 Previous issue date: 2009en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348882-
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordEndogenouspt_BR
dc.identifier.source000261132100001pt_BR
dc.creator.orcidSem informaçãopt_BR
dc.type.formArtigo originalpt_BR
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