Gene Expression Control by Glucocorticoid Receptors during Innate Immune Responses

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dc.citation.volume7
dc.contributor.authorXavier, Andre Machado [UNIFESP]
dc.contributor.authorAnunciato, Aparecida Kataryna Olimpio [UNIFESP]
dc.contributor.authorRosenstock, Tatiana Rosado
dc.contributor.authorGlezer, Isaias [UNIFESP]
dc.coverageLausanne
dc.date.accessioned2020-07-22T13:23:07Z
dc.date.available2020-07-22T13:23:07Z
dc.date.issued2016
dc.description.abstractGlucocorticoids (GCs) are potent anti-inflammatory compounds that have been extensively used in clinical practice for several decades. GC's effects on inflammation are generally mediated through GC receptors (GRs). Signal transduction through these nuclear receptors leads to dramatic changes in gene expression programs in different cell types, typically due to GR binding to DNA or to transcription modulators. During the last decade, the view of GCs as exclusive anti-inflammatory molecules has been challenged. GR negative interference in pro-inflammatory gene expression was a landmark in terms of molecular mechanisms that suppress immune activity. In fact, GR can induce varied inhibitory molecules, including a negative regulator of Toll-like receptors pathway, or subject key transcription factors, such as NF-kappa B and AP-1, to a repressor mechanism. In contrast, the expression of some acute-phase proteins and other players of innate immunity generally requires GR signaling. Consequently, GRs must operate context-dependent inhibitory, permissive, or stimulatory effects on host defense signaling triggered by pathogens or tissue damage. This review aims to disclose how contradictory or comparable effects on inflammatory gene expression can depend on pharmacological approach (including selective GC receptor modulatorsen
dc.description.abstractSEGRMs), cell culture, animal treatment, or transgenic strategies used as models. Although the current view of GR-signaling integrated many advances in the field, some answers to important questions remain elusive.en
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Biochem, Sao Paulo, Brazil
dc.description.affiliationSanta Casa Sao Paulo Med Sch, Dept Physiol Sci, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Biochem, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo
dc.description.sponsorshipConselho National de Desenvolvimento Cientifico e TecnolOgico
dc.description.sponsorshipIDFAPESP: 2007/53732-8
dc.description.sponsorshipIDCNPq: 484869/2012-4
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.3389/fendo.2016.00031
dc.identifier.citationFrontiers In Endocrinology. Lausanne, v. 7, p. -, 2016.
dc.identifier.doi10.3389/fendo.2016.00031
dc.identifier.fileWOS000378508300001.pdf
dc.identifier.issn1664-2392
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/56048
dc.identifier.wosWOS:000378508300001
dc.language.isoeng
dc.publisherFrontiers Media Sa
dc.relation.ispartofFrontiers In Endocrinology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectacute-phase responseen
dc.subjectcortisolen
dc.subjectgene expressionen
dc.subjectinflammatory diseasesen
dc.subjectinnate immune responseen
dc.subjectGREen
dc.subjectSEGRAsen
dc.subjecttransrepressionen
dc.titleGene Expression Control by Glucocorticoid Receptors during Innate Immune Responsesen
dc.typeinfo:eu-repo/semantics/article
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