Anti-inflammatory functions of glucocorticoid-induced genes

Clark, Andrew R.

doi:10.1016/j.mce.2007.04.013

Cited by 232 publications

(202 citation statements)

References 299 publications

(325 reference statements)

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“…They are indicated by names at their spot positions in the gels. These proteins showed much higher expression levels in RA than in healthy control function as a cellular mediator of the anti-inflammatory actions of GCs [13]. Moreover, recent evidences show that Anx-1 exerts endogenous anti-inflammatory effects on adjuvant-induced arthritis via the regulation of cytokine gene expression in the synovium.…”

Section: Discussionmentioning

confidence: 98%

Analyses of differential proteome of human synovial fibroblasts obtained from arthritis

Zhou

Wang

et al. 2008

Clin Rheumatol

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There is mounting evidence indicating that the synovial fibroblasts (SFs) contribute to the pathogenesis of rheumatoid arthritis (RA). The present study showed the differential proteins expression pattern of SFs from patients with RA or osteoarthritis (OA) and healthy control. Cellular proteins of cultured SFs were subjected to 2-DE and visualized by silver nitrate staining. A total of 49 spots that were statistically and differentially overexpressed in RA or OA in comparison to healthy ones were identified by MALDI-TOF-MS, and 25 proteins were successfully identified. Western blot was used to further verify some of the differential proteins. These proteins included enzymatic and structural proteins, signal transduction proteins, calcium binding protein, etc. From all of the identified proteins, a number of proteins have been implicated that involved in the healthy or pathological SFs function (e.g., S100A4, S100A10, cathepsin D) or that have potential diagnostic and prognostic value for RA (α-enolase and TPI) or that may be the new therapeutic targets (Annexin, SOD, PRX).

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Section: Discussionmentioning

confidence: 98%

Analyses of differential proteome of human synovial fibroblasts obtained from arthritis

Zhou

Wang

et al. 2008

Clin Rheumatol

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“…60). Therefore, defective induction of these GR-dependent genes might account for the reduced repression of inflammatory genes after TNF␣ stimulation.…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor Inhibits Glucocorticoid Receptor Function in Mice

Bogaert

Vandevyver

Dejager

et al. 2011

Journal of Biological Chemistry

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As glucocorticoid resistance (GCR) and the concomitant burden pose a worldwide problem, there is an urgent need for a more effective glucocorticoid therapy, for which insights into the molecular mechanisms of GCR are essential. In this study, we addressed the hypothesis that TNF␣, a strong pro-inflammatory mediator in numerous inflammatory diseases, compromises the protective function of the glucocorticoid receptor (GR) against TNF␣-induced lethal inflammation. Indeed, protection of mice by dexamethasone against TNF␣ lethality was completely abolished when it was administered after TNF␣ stimulation, indicating compromised GR function upon TNF␣ challenge. TNF␣-induced GCR was further demonstrated by impaired GR-dependent gene expression in the liver. Furthermore, TNF␣ down-regulates the levels of both GR mRNA and protein. However, this down-regulation seems to occur independently of GC production, as TNF␣ also resulted in downregulation of GR levels in adrenalectomized mice. These findings suggest that the decreased amount of GR determines the GR response and outcome of TNF␣-induced shock, as supported by our studies with GR heterozygous mice. We propose that by inducing GCR, TNF␣ inhibits a major brake on inflammation and thereby amplifies the pro-inflammatory response. Our findings might prove helpful in understanding GCR in inflammatory diseases in which TNF␣ is intimately involved.

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“…The immunosuppressive effects of GR signalling include inhibition of transcription factors such as nuclear factor kB (NFkB) and activating protein 1 (Clark 2007), suppression of inflammatory prostaglandins (Bailey 1991) and induction of apoptosis in T and B lymphocytes (Tuckermann et al 2005). In macrophages, glucocorticoid exposure alters the expression of many pro-and anti-inflammatory genes (Ehrchen et al 2007) and promotes phagocytosis of apoptotic cells (Liu et al 1999).…”

Section: Grs Macrophages and Diseasementioning

confidence: 99%

Corticosteroid receptors, macrophages and cardiovascular disease

Rickard¹,

Young²

2009

Journal of Molecular Endocrinology

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The mineralocorticoid receptor (MR) and glucocorticoid receptor are ligand-activated transcription factors that have important physiological and pathophysiological actions in a broad range of cell types including monocytes and macrophages. While the glucocorticoids cortisol and corticosterone have well-described anti-inflammatory actions on both recruited and tissue resident macrophages, a role for the mineralocorticoid aldosterone in these cells is largely undefined. Emerging evidence, however, suggests that MR signalling may promote pro-inflammatory effects. This review will discuss the current understanding of the role of corticosteroid receptors in macrophages and their effect on diseases involving inflammation, with a particular focus on cardiovascular disease.

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Anti-inflammatory functions of glucocorticoid-induced genes

Cited by 232 publications

References 299 publications

Analyses of differential proteome of human synovial fibroblasts obtained from arthritis

Analyses of differential proteome of human synovial fibroblasts obtained from arthritis

Tumor Necrosis Factor Inhibits Glucocorticoid Receptor Function in Mice

Corticosteroid receptors, macrophages and cardiovascular disease

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