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Temporal gene expression in the hippocampus and peripheral organs to endotoxin-induced systemic inflammatory response in caspase-1-deficient mice

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dc.creatorMastronardi, Claudio Albertospa
dc.creatorPaz-Filho, Gilbertospa
dc.creatorZanoni, Martinaspa
dc.creatorMolano González, Nicolás
dc.creatorArcos-Burgos, Mauriciospa
dc.creatorLicinio, Juliospa
dc.creatorWong, Ma-Lispa
dc.date.accessioned2020-05-25T23:57:22Z
dc.date.available2020-05-25T23:57:22Z
dc.date.created2015spa
dc.description.abstractObjectives: Caspase-1 (casp1), a key protease involved in the systemic inflammatory response syndrome (SIRS), controls the brain expression of a set of eight genes: Nos2 and Ptgs2 (nitric oxide synthase 2 and prostaglandin-endoperoxide synthase 2, two inducible enzymes), Cxcl1 and Cxcl10 (C-X-C motif chemokine ligand 1 and ligand 10), Tgtp and Gbp2 (T cell-specific GTPase 1 and guanylate-binding protein 2, two GTPases), Adamts1 (a disintegrin-like and metallopeptidase with thrombospondin type 1 motif, 1, a metalloprotease) and Il1rn (interleukin-1 receptor antagonist). Our objective was to ascertain whether casp1 also controlled the peripheral expression of these genes and, if so, to compare their central versus peripheral patterns of gene expression in immune and endocrine tissues during SIRS. Methods: Wild-type (wt) and casp1 knockout (casp1-/-) mice were injected with either saline or a high dose of endotoxin/lipopolysaccharide (LPS; 800 ?g/mice i.p.). Saline-injected mice were immediately euthanized after injection, whereas LPS-injected mice were sacrificed 6 and 12 h after LPS administration. Hippocampal, splenic and adrenal gene expressions were determined by real-time PCR. Results: Overall, casp1-/- mice showed a lower inflammatory response than wt mice. The expression levels of powerful proinflammatory factors such as Nos2 and Ptgs2 was reduced in casp1-/- mice. Moreover, a hierarchical clustering analysis aimed at studying patterns of gene coexpression revealed large alterations in the hippocampal pattern of casp1-/- mice. Surprisingly, the expression of Adamts1 was increased in the hippocampus and adrenals of casp1-/- mice. Conclusions: The resilience of casp1-/- mice to SIRS lethality is associated with a lower inflammatory response, loss of hippocampal gene coexpression patterns, and increased hippocampal Adamts1 gene expression. The latter might be beneficial for casp1-/- mice, since ADAMTS1 is likely to play a role in neuronal plasticity. The mechanisms described here may help the development of either novel biomarkers or therapeutic targets against SIRS/sepsis. © 2015 S. Karger AG, Basel.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1159/000368310
dc.identifier.issn14230216
dc.identifier.issn10217401
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/22651
dc.language.isoengspa
dc.publisherS. Karger AGspa
dc.relation.citationEndPage273
dc.relation.citationIssueNo. 4
dc.relation.citationStartPage263
dc.relation.citationTitleNeuroImmunoModulation
dc.relation.citationVolumeVol. 22
dc.relation.ispartofNeuroImmunoModulation, ISSN:14230216, 10217401, Vol.22, No.4 (2015); pp. 263-273spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84928418148&doi=10.1159%2f000368310&partnerID=40&md5=021ec49901a9b05a8c397e0e4f6a01cdspa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordEndotoxinspa
dc.subject.keywordEscherichia coli lipopolysaccharidespa
dc.subject.keywordSodium chloridespa
dc.subject.keywordInterleukin 1beta converting enzymespa
dc.subject.keywordLipopolysaccharidespa
dc.subject.keywordAdamts1 genespa
dc.subject.keywordAdrenal glandspa
dc.subject.keywordAnimal experimentspa
dc.subject.keywordAnimal modelspa
dc.subject.keywordAnimal tissuespa
dc.subject.keywordArticlespa
dc.subject.keywordCaspase 1 genespa
dc.subject.keywordControlled studyspa
dc.subject.keywordCorrelation coefficientspa
dc.subject.keywordCxc motif ligand 1 genespa
dc.subject.keywordCxc motif ligand 10 genespa
dc.subject.keywordDisintegrin like and metallopeptidase with thrombospondin type 1 motif 1 genespa
dc.subject.keywordGene expression profilingspa
dc.subject.keywordGene inactivationspa
dc.subject.keywordGene interactionspa
dc.subject.keywordGenetic associationspa
dc.subject.keywordGuanylate binding protein 2 genespa
dc.subject.keywordHippocampusspa
dc.subject.keywordImmune response genespa
dc.subject.keywordImmunogeneticsspa
dc.subject.keywordInducible nitric oxide synthase genespa
dc.subject.keywordInflammationspa
dc.subject.keywordInjectionspa
dc.subject.keywordInterleukin 1 receptor antagonist genespa
dc.subject.keywordLethalityspa
dc.subject.keywordMalespa
dc.subject.keywordMousespa
dc.subject.keywordNerve cell plasticityspa
dc.subject.keywordNonhumanspa
dc.subject.keywordPriority journalspa
dc.subject.keywordProstaglandin endoperoxide synthase 2 genespa
dc.subject.keywordReal time polymerase chain reactionspa
dc.subject.keywordSpleenspa
dc.subject.keywordSystemic inflammatory response syndromespa
dc.subject.keywordT cell specific gtpase 1 genespa
dc.subject.keywordWild typespa
dc.subject.keywordAdrenal glandspa
dc.subject.keywordAnimalspa
dc.subject.keywordC57bl mousespa
dc.subject.keywordChemically inducedspa
dc.subject.keywordDeficiencyspa
dc.subject.keywordDisease modelspa
dc.subject.keywordGene expressionspa
dc.subject.keywordGeneticsspa
dc.subject.keywordHippocampusspa
dc.subject.keywordKnockout mousespa
dc.subject.keywordMetabolismspa
dc.subject.keywordSpleenspa
dc.subject.keywordSystemic inflammatory response syndromespa
dc.subject.keywordAdrenal glandsspa
dc.subject.keywordAnimalsspa
dc.subject.keywordCaspase 1spa
dc.subject.keywordDisease modelseng
dc.subject.keywordGene expressionspa
dc.subject.keywordHippocampusspa
dc.subject.keywordLipopolysaccharidesspa
dc.subject.keywordMalespa
dc.subject.keywordMicespa
dc.subject.keywordMiceeng
dc.subject.keywordMiceeng
dc.subject.keywordSpleenspa
dc.subject.keywordSystemic inflammatory response syndromespa
dc.subject.keywordAdamts1spa
dc.subject.keywordChemokinesspa
dc.subject.keywordCoexpressionspa
dc.subject.keywordCox2spa
dc.subject.keywordCxcl1spa
dc.subject.keywordCxcl10spa
dc.subject.keywordInflammationspa
dc.subject.keywordLipopolysaccharidespa
dc.subject.keywordNos2spa
dc.subject.keywordTranscriptionspa
dc.titleTemporal gene expression in the hippocampus and peripheral organs to endotoxin-induced systemic inflammatory response in caspase-1-deficient micespa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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