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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampHomsi, Eduardo-
dc.contributor.authorunicampFaria, Jose Butori Lopes de-
dc.typeArtigopt_BR
dc.titleTNF-alpha-mediated cardiorenal injury after rhabdomyolysis in ratspt_BR
dc.contributor.authorHomsi, Eduardo-
dc.contributor.authorAndreazzi, Diego Duarte-
dc.contributor.authorLopes de Faria, Jose Butori-
dc.contributor.authorJanino, Patricia-
dc.subjectLesão renal agudapt_BR
dc.subjectApoptosept_BR
dc.subjectFator de necrose tumoral alfapt_BR
dc.subjectRabdomiólisept_BR
dc.subject.otherlanguageAcute kidney injurypt_BR
dc.subject.otherlanguageApoptosispt_BR
dc.subject.otherlanguageTumor necrosis factor-alphapt_BR
dc.subject.otherlanguageRhabdomyolysispt_BR
dc.description.abstractThe TNF-alpha serum level increases after rhabdomyolysis and is involved in the subsequent cardiorenal injury. In the present study, we investigated the TNF-alpha dependent cell signaling pathways implicated in cellular injury in these organs. Rhabdomyolysis was induced by intramuscular glycerol injection in rats. Renal function, cardiac and renal pathology, and activation of caspases were evaluated during the first 24 h after glycerol injection. TNF-alpha blockade with infliximab reduced tubular necrosis and cardiorenal apoptosis. Cellular Fas-associated protein with death domain-like IL-1 beta-converting enzyme inhibitory protein (cFLIP), an inhibitor of caspase-8, was overexpressed in the kidney but not in the heart. The inhibitory effect of cFLIP blunted caspase-8 activation in the kidney. In this condition, the cellular response to the TNF-alpha stimulus was driven to receptor-interacting protein-1 (RIP1)-mediated necroptosis. Treatment with RIP1 inhibitor (necrostatin-1) isolated or in combination with infliximab showed a similar reduction in tubular necrosis, underscoring the importance of TNF-alpha-mediated tubular necroptosis in this model. TNF-alpha played a positive regulatory role in the transcription of proapoptotic Bax and p53-upregulated modulator of apoptosis (PUMA) proteins. Infliximab treatment reduced caspase-9-mediated apoptosis in both organs. Treatment with a caspase-8 inhibitor showed that caspase-8 participated in the process of apoptosis only in the heart, upstream of caspase-9 activation. TNF-alpha-mediated necroptosis is the predominant form of tubular injury observed in the glycerol model. TNF-alpha up regulates Bax and PUMA proapoptotic proteins, resulting in activation of the intrinsic pathway of apoptosis in the kidney and heartpt_BR
dc.relation.ispartofAmerican journal of physiology: renal physiologypt_BR
dc.relation.ispartofabbreviationAm. j. physiol. renal. physiol.pt_BR
dc.publisher.cityRockville, MDpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherAmerican Physiological Societypt_BR
dc.date.issued2015-
dc.date.monthofcirculationJunept_BR
dc.language.isoengpt_BR
dc.description.volume308pt_BR
dc.description.issuenumber11pt_BR
dc.description.firstpageF1259pt_BR
dc.description.lastpageF1267pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1931-857Xpt_BR
dc.identifier.eissn1522-1466pt_BR
dc.identifier.doi10.1152/ajprenal.00311.2014pt_BR
dc.identifier.urlhttps://journals.physiology.org/doi/full/10.1152/ajprenal.00311.2014pt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumberFundo de Apoio ao Ensino, a Pesquisa e Extensao/Universidade Estadual de Campinas (Campinas, Brazil)pt_BR
dc.date.available2021-02-11T18:02:46Z-
dc.date.accessioned2021-02-11T18:02:46Z-
dc.description.provenanceSubmitted by Cintia Oliveira de Moura (cintiaom@unicamp.br) on 2021-02-11T18:02:46Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-05-25T14:37:24Z : No. of bitstreams: 1 000356237200009.pdf: 6073916 bytes, checksum: 71381ffe8db652fe4f702183f5e0ab99 (MD5)en
dc.description.provenanceMade available in DSpace on 2021-02-11T18:02:46Z (GMT). No. of bitstreams: 0 Previous issue date: 2015en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/355630-
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000356237200009pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0003-2373-5539pt_BR
dc.type.formArtigopt_BR
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