Nongenomic glucocorticoid signaling: New targets for immunosuppressive therapy?

Schoneveld, J. Leonard M.; Fritsch-Stork, Ruth; Bijlsma, J. W. J.

doi:10.1002/art.30635

Cited by 7 publications

(1 citation statement)

References 10 publications

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“…The later is faster and less characterized. Although probable, there are no strong evidences that GR engage relevant non-genomic signal transduction to repress pro-inflammatory signaling during innate immune responses ( 41 , 42 ). GR genomic mechanisms that inhibit pro-inflammatory signaling include: (1) direct transcription of genes that will negatively interfere with pathways involved in the synthesis of inflammatory mediators; (2) direct repression of genes that contribute to immune cells activation; (3) negative interference in transcriptional events engaged by transcriptions factors that transduce pro-inflammatory signals; and (4) synergism between GR and other transcription factors activated during inflammation, ultimately promoting the induction of “anti-inflammatory” gene products.…”

Section: Gr Repression On Pro-inflammatory Genesmentioning

confidence: 99%

Gene Expression Control by Glucocorticoid Receptors during Innate Immune Responses

et al. 2016

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Glucocorticoids (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-κB 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 modulators; SEGRMs), 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.

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Section: Gr Repression On Pro-inflammatory Genesmentioning

confidence: 99%

Gene Expression Control by Glucocorticoid Receptors during Innate Immune Responses

et al. 2016

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Glucocorticoids and the Cardiovascular System

Goodwin

2015

Advances in Experimental Medicine and Biology

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Glucocorticoids affect the developing and mature cardiovascular system in profound and, at times, contradictory ways. The glucocorticoid receptor is ubiquitous in most cell types and conserved across species, highlighting its importance in development and homeostasis. Despite the fact that the glucocorticoid receptor is widely expressed, tissue-specific effects of glucocorticoids may have pronounced effects on whole organism phenotypes. Here we will review the interactions between glucocorticoids and the cardiovascular system.

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Immunopathology of the Endocrine System

Rosol

Walling

2017

Immunopathology in Toxicology and Drug Development

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Nongenomic glucocorticoid signaling: New targets for immunosuppressive therapy?

Cited by 7 publications

References 10 publications

Gene Expression Control by Glucocorticoid Receptors during Innate Immune Responses

Gene Expression Control by Glucocorticoid Receptors during Innate Immune Responses

Glucocorticoids and the Cardiovascular System

Immunopathology of the Endocrine System

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