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dc.contributor.authorBobermin, Larissa Danielept_BR
dc.contributor.authorQuincozes-Santos, Andrépt_BR
dc.contributor.authorSantos, Camila Leitept_BR
dc.contributor.authorVarela, Ana Paula Muterlept_BR
dc.contributor.authorTeixeira, Thais Fumacopt_BR
dc.contributor.authorWartchow, Krista Minéiapt_BR
dc.contributor.authorLissner, Lílian Julianapt_BR
dc.contributor.authorSilva, Amanda dapt_BR
dc.contributor.authorThomaz, Natalie Katherinept_BR
dc.contributor.authorSanti, Lucéliapt_BR
dc.contributor.authorSilva, Walter Orlando Beys dapt_BR
dc.contributor.authorRoehe, Paulo Michelpt_BR
dc.contributor.authorSesterheim, Patríciapt_BR
dc.contributor.authorGuimaraes, Jorge Almeidapt_BR
dc.contributor.authorGoncalves, Carlos Alberto Saraivapt_BR
dc.contributor.authorSouza, Diogo Onofre Gomes dept_BR
dc.date.accessioned2021-01-13T04:10:32Zpt_BR
dc.date.issued2020pt_BR
dc.identifier.issn2045-2322pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/217251pt_BR
dc.description.abstractZika virus (ZIKV) infection during pregnancy was associated with microcephaly in neonates, but clinical and experimental evidence indicate that ZIKV also causes neurological complications in adults. However, the changes in neuron-glial communication, which is essential for brain homeostasis, are still unknown. Here, we report that hippocampal slices from adult rats exposed acutely to ZIKV showed significant cellular alterations regarding to redox homeostasis, inflammatory process, neurotrophic functions and molecular signalling pathways associated with neurons and glial cells. Our findings support the hypothesis that ZIKV is highly neurotropic and its infection readily induces an inflammatory response, characterized by an increased expression and/or release of pro-inflammatory cytokines. We also observed changes in neural parameters, such as adenosine receptor A2a expression, as well as in the release of brain-derived neurotrophic factor and neuron-specific enolase, indicating plasticity synaptic impairment/neuronal damage. In addition, ZIKV induced a glial commitment, with alterations in specific and functional parameters such as aquaporin 4 expression, S100B secretion and glutathione synthesis. ZIKV also induced p21 senescence-associated gene expression, indicating that ZIKV may induce early senescence. Taken together, our results indicate that ZIKV-induced neuroinflammation, involving nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor κB (NFκB) pathways, affects important aspects of neuron-glia communication. Therefore, although ZIKV infection is transient, long-term consequences might be associated with neurological and/or neurodegenerative diseases.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofScientific reports. London. Vol. 10 (2020), 21604, 11 p.pt_BR
dc.rightsOpen Accessen
dc.subjectInfecção por Zika viruspt_BR
dc.subjectNeurogliapt_BR
dc.subjectHipocampopt_BR
dc.subjectNF-kappa Bpt_BR
dc.subjectComunicação celularpt_BR
dc.titleZika virus exposure affects neuron-glia communication in the hippocampal slices of adult ratspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001121115pt_BR
dc.type.originEstrangeiropt_BR


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