Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/353148
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampOliveira, Helena Coutinho Franco de-
dc.contributor.authorunicampVercesi, Anibal Eugenio-
dc.typeArtigopt_BR
dc.titleLiver proteomic response to hypertriglyceridemia in human-apolipoprotein C-III transgenic mice at cellular and mitochondrial compartment levelspt_BR
dc.contributor.authorEhx, Grégory-
dc.contributor.authorGérin, Stéphanie-
dc.contributor.authorMathy, Grégory-
dc.contributor.authorFranck, Fabrice-
dc.contributor.authorOliveira, Helena C. F.-
dc.contributor.authorVercesi, Anibal E.-
dc.contributor.authorSluse, Francis E.-
dc.subjectHipertrigliceridemiapt_BR
dc.subject.otherlanguageHypertriglyceridemiapt_BR
dc.description.abstractBackground Hypertriglyceridemia (HTG) is defined as a triglyceride (TG) plasma level exceeding 150 mg/dl and is tightly associated with atherosclerosis, metabolic syndrome, obesity, diabetes and acute pancreatitis. The present study was undertaken to investigate the mitochondrial, sub-mitochondrial and cellular proteomic impact of hypertriglyceridemia in the hepatocytes of hypertriglyceridemic transgenic mice (overexpressing the human apolipoproteinC-III). Methods Quantitative proteomics (2D-DIGE) analysis was carried out on both “low-expressor” (LE) and “high-expressor” (HE) mice, respectively exhibiting moderate and severe HTG, to characterize the effect of the TG plasma level on the proteomic response. Results The mitoproteome analysis has revealed a large-scale phenomenon in transgenic mice, i.e. a general down-regulation of matricial proteins and up-regulation of inner membrane proteins. These data also demonstrate that the magnitude of proteomic changes strongly depends on the TG plasma level. Our different analyses indicate that, in HE mice, the capacity of several metabolic pathways is altered to promote the availability of acetyl-CoA, glycerol-3-phosphate, ATP and NADPH for TG de novo biosynthesis. The up-regulation of several cytosolic ROS detoxifying enzymes has also been observed, suggesting that the cytoplasm of HTG mice is subjected to oxidative stress. Moreover, our results suggest that iron over-accumulation takes place in the cytosol of HE mice hepatocytes and may contribute to enhance oxidative stress and to promote cellular proliferation. Conclusions These results indicate that the metabolic response to HTG in human apolipoprotein C-III overexpressing mice may support a high TG production rate and that the cytosol of hepatocytes is subjected to an important oxidative stress, probably as a result of FFA over-accumulation, iron overload and enhanced activity of some ROS-producing catabolic enzymespt_BR
dc.relation.ispartofLipids in health and diseasept_BR
dc.relation.ispartofabbreviationLipids health dis.pt_BR
dc.publisher.cityLondonpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherSpringer Naturept_BR
dc.date.issued2014-
dc.language.isoengpt_BR
dc.description.volume13pt_BR
dc.rightsAbertopt_BR
dc.sourceSCOPUSpt_BR
dc.identifier.eissn1476-511Xpt_BR
dc.identifier.doi10.1186/1476-511X-13-116pt_BR
dc.identifier.urlhttps://lipidworld.biomedcentral.com/articles/10.1186/1476-511X-13-116pt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumber2011/50400-0pt_BR
dc.date.available2020-12-14T12:16:39Z-
dc.date.accessioned2020-12-14T12:16:39Z-
dc.description.provenanceSubmitted by Sanches Olivia (olivias@unicamp.br) on 2020-12-14T12:16:39Z No. of bitstreams: 0en
dc.description.provenanceMade available in DSpace on 2020-12-14T12:16:39Z (GMT). No. of bitstreams: 0 Previous issue date: 2014en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/353148-
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.departmentDepartamento de Patologia Clínicapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordNASHpt_BR
dc.subject.keywordProtein spotpt_BR
dc.subject.keywordUrea cyclept_BR
dc.subject.keywordMitoKATP channelpt_BR
dc.subject.keywordHepatic iron overloadpt_BR
dc.identifier.source2-s2.0-84904448121pt_BR
dc.creator.orcid0000-0003-0119-6992pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.type.formArtigo de pesquisapt_BR
dc.identifier.articleid116pt_BR
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