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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampVendramini-Costa, Débora Barbosa-
dc.typeArtigopt_BR
dc.titleExpression patterns of sirtuin 1-AMPK-autophagy pathway in chronic colitis and inflammation-associated colon neoplasia in IL-10-deficient micept_BR
dc.contributor.authorTalero, Elena-
dc.contributor.authorAlcaide, Antonio-
dc.contributor.authorÁvila-Román, Javier-
dc.contributor.authorGarcía-Mauriño, Sofía-
dc.contributor.authorVendramini-Costa, Débora-
dc.contributor.authorMotilva, Virginia-
dc.subjectSirtuína 1pt_BR
dc.subjectAutofagiapt_BR
dc.subject.otherlanguageSirtuin 1pt_BR
dc.subject.otherlanguageAutophagypt_BR
dc.description.abstractInterleukin-10-deficient (IL-10 (−/−)) mice spontaneously develop chronic colitis and adenocarcinoma through the dysplasia sequence. Autophagy malfunction is associated to inflammatory bowel disease (IBD) and colorectal cancer (CRC) pathogenesis. Autophagy is regulated by silent information regulator-1 (SIRT1), a NAD +-dependent histone deacetylase. Our aim was to investigate the expression changes of SIRT1-AMPK-autophagy pathway in the progression from chronic colitis to CRC. We studied C57BL/6-IL-10-deficient mice between 6 and 18 weeks of age. Macroscopic and histological analysis, and characterization of inflammatory and tumor biomarkers were performed. IL-10-deficient mice developed colitis from the age of 6 weeks onward. The severity of inflammation and dysplasia, and the proliferative activity increased gradually with age. IL-10 (−/−) mice were characterized by improved levels of TNF-α and decreased expression of SIRT1. Moreover, our findings show an increase in p-AMPK expression and an activation of the autophagy in IL-10 (−/−) mice from all stages, evidenced by the accumulation of LC3-II protein, the increase in Beclin 1 expression and the reduction in Bcl-2 levels. SIRT1-AMPK-autophagy pathway may be involved in the maintenance of chronic inflammation and dysplasia development in the IL-10-deficient mice model. Modulation of this pathway could be a novel strategy for IBD and CRC treatmentpt_BR
dc.relation.ispartofInternational immunopharmacologypt_BR
dc.relation.ispartofabbreviationInt. immunopharmacol.pt_BR
dc.publisher.cityLondonpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherElsevierpt_BR
dc.date.issued2016-
dc.date.monthofcirculationJunept_BR
dc.language.isoengpt_BR
dc.description.volume35pt_BR
dc.description.firstpage248pt_BR
dc.description.lastpage256pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1567-5769pt_BR
dc.identifier.eissn1878-1705pt_BR
dc.identifier.doi10.1016/j.intimp.2016.03.046pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S1567576916301321pt_BR
dc.date.available2020-09-29T14:21:01Z-
dc.date.accessioned2020-09-29T14:21:01Z-
dc.description.provenanceSubmitted by Mariana Aparecida Azevedo (mary1@unicamp.br) on 2020-09-29T14:21:01Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-02-17T13:00:13Z : No. of bitstreams: 1 000376212500030.pdf: 2215845 bytes, checksum: c632dd57bd606afe9bbdf58b696f9399 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-29T14:21:01Z (GMT). No. of bitstreams: 0 Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/350145-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.subject.keywordChronic inflammationpt_BR
dc.subject.keywordColon carcinogenesispt_BR
dc.subject.keywordIL-10-deficient micept_BR
dc.identifier.source000376212500030pt_BR
dc.creator.orcid0000-0001-7617-4945pt_BR
dc.type.formArtigopt_BR
dc.description.sponsorNoteThis work was supported by Consejería de Innovación, Ciencia y Empresa-Junta de Andalucía (P09-AGR-5185, Polfanat). We thank “Centro de Investigación, Tecnología e Innovación (CITIUS)” of the University of Seville for providing technical assistancept_BR
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