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dc.contributor.authorGuimarães, Natália C.-
dc.contributor.authorAlves, Débora S.-
dc.contributor.authorVilela, Wembley R.-
dc.contributor.authorFerreira, Eduardo de Souza-
dc.contributor.authorGomes, Bruna R. B.-
dc.contributor.authorOtt, Daniela-
dc.contributor.authorMurgott, Jolanta-
dc.contributor.authorSouza, Paulo Eduardo Narcizo de-
dc.contributor.authorSousa, Marcelo V. de-
dc.contributor.authorGalina, Antonio-
dc.contributor.authorRoth, Joachim-
dc.contributor.authorFabro de Bem, Andreza-
dc.contributor.authorSouza, Fabiane Hiratsuka Veiga de-
dc.date.accessioned2021-06-08T12:51:23Z-
dc.date.available2021-06-08T12:51:23Z-
dc.date.issued2021-
dc.identifier.citationGUIMARÃES, Natália C. et al. Mitochondrial pyruvate carrier as a key regulator of fever and neuroinflammation. Brain, Behavior, and Immunity, v. 92, p. 90-101, 2021. DOI: https://doi.org/10.1016/j.bbi.2020.11.031.pt_BR
dc.identifier.urihttps://repositorio.unb.br/handle/10482/41114-
dc.language.isoInglêspt_BR
dc.publisherElsevier Inc.pt_BR
dc.rightsAcesso Restritopt_BR
dc.titleMitochondrial pyruvate carrier as a key regulator of fever and neuroinflammationpt_BR
dc.typeArtigopt_BR
dc.subject.keywordHipotálamopt_BR
dc.subject.keywordInflamaçãopt_BR
dc.subject.keywordMitocôndriapt_BR
dc.subject.keywordNeurometabolismopt_BR
dc.identifier.doihttps://doi.org/10.1016/j.bbi.2020.11.031pt_BR
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/abs/pii/S0889159120324077?via%3Dihubpt_BR
dc.description.abstract1The mitochondrial pyruvate carrier (MPC) is an inner-membrane transporter that facilitates pyruvate uptake from the cytoplasm into mitochondria. We previously reported that MPC1 protein levels increase in the hypothalamus of animals during fever induced by lipopolysaccharide (LPS), but how this increase contributes to the LPS responses remains to be studied. Therefore, we investigated the effect of UK 5099, a classical MPC inhibitor, in a rat model of fever, on hypothalamic mitochondrial function and neuroinflammation in LPS-stimulated preoptic area (POA) primary microcultures. Intracerebroventricular administration of UK 5099 reduced the LPS-induced fever. High-resolution respirometry revealed an increase in oxygen consumption and oxygen flux related to ATP synthesis in the hypothalamic homogenate from LPS-treated animals linked to mitochondrial complex I plus II. Preincubation with UK 5099 prevented the LPS-induced increase in oxygen consumption, ATP synthesis and spare capacity only in complex I-linked respiration and reduced mitochondrial H2O2 production. In addition, treatment of rat POA microcultures with UK 5099 reduced the secretion of the proinflammatory and pyrogenic cytokines TNFα and IL-6 as well as the immunoreactivity of inflammatory transcription factors NF-κB and NF-IL6 four hours after LPS stimulation. These results suggest that the regulation of mitochondrial pyruvate metabolism through MPC inhibition may be effective in reducing neuroinflammation and fever.pt_BR
Collection(s) :CEL - Artigos publicados em periódicos
CFS - Artigos publicados em periódicos
FCE-FAR - Artigos publicados em periódicos
IF - Artigos publicados em periódicos

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