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Genomic Redistribution of GR Monomers and Dimers Mediates the Transcriptional Response to Exogenous Glucocorticoid In Vivo.

ABSTRACT: Expression profiles of GRdim mutant macrophages (mouse, bone-marrow derived) treated with LPS for 6 hrs or with LPS (6hrs) + Dex (O/N 1uM). Identification of GR-regulated genes in response to LPS.

ORGANISM(S): Mus musculus

PROVIDER: GSE68160 | GEO | 2015/04/23

SECONDARY ACCESSION(S): PRJNA281933

REPOSITORIES: GEO

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Genomic Redistribution of GR Monomers and Dimers Mediates the Transcriptional Response to Exogenous Glucocorticoid In Vivo.

Project description:Expression profiles of GRdim mutant macrophages (mouse, bone-marrow derived) treated with LPS for 6 hrs or with LPS (6hrs) + Dex (O/N 1uM). Identification of GR-regulated genes in response to LPS. 3 Grdim mutant macrophages samples treated with LPS (6hrs) and 3 Grdim mutant macrophage samples treated with LPS (6hrs) and Dex (overnight).

2015-04-23 | E-GEOD-68160 | biostudies-arrayexpress

Genomic redistribution of GR monomers and dimers mediates transcriptional response to exogenous glucocorticoid in vivo.

Project description:Glucocorticoids (GCs) are commonly prescribed drugs, but their anti-inflammatory benefits are mitigated by metabolic side effects. Their transcriptional effects, including tissue-specific gene activation and repression, are mediated by the glucocorticoid receptor (GR), which is known to bind as a homodimer to a palindromic DNA sequence. Using ChIP-exo in mouse liver under endogenous corticosterone exposure, we report here that monomeric GR interaction with a half-site motif is more prevalent than homodimer binding. Monomers colocalize with lineage-determining transcription factors in both liver and primary macrophages, and the GR half-site motif drives transcription, suggesting that monomeric binding is fundamental to GR's tissue-specific functions. In response to exogenous GC in vivo, GR dimers assemble on chromatin near ligand-activated genes, concomitant with monomer evacuation of sites near repressed genes. Thus, pharmacological GCs mediate gene expression by favoring GR homodimer occupancy at classic palindromic sites at the expense of monomeric binding. The findings have important implications for improving therapies that target GR.

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Glucocorticoid receptor dimers control intestinal STAT1-mediated IFN- and TNF-induced inflammation in mice

Project description:Tumor Necrosis Factor (TNF) is an important mediator in numerous inflammatory diseases, e.g. in inflammatory bowel diseases (IBD). In IBD, acute increases in TNF production can lead to disease flares. Glucocorticoids (GCs), which are steroids that bind and activate the glucocorticoid receptor (GR), are able to protect animals and humans against acute TNF-induced inflammatory symptoms. Mice with a poor transcriptional response of GR-dimer-dependent target genes were studied in a model of TNF-induced lethal inflammation. In contrast to the GRwt/wt mice, these GRdim/dim mice displayed a significant increase in TNF sensitivity and a lack of protection by the GC dexamethasone (DEX). Unchallenged GRdim/dim mice had a strong interferon-stimulated gene (ISG) signature, along with STAT1 upregulation and phosphorylation. This ISG signature was gut specific and, based on our studies with antibiotics, depended on the gut microbiota. GR dimers directly bound to short DNA sequences in the STAT1 promoter known as inverted repeat negative GRE (IR-nGRE) elements. Poor control of STAT1 in GRdim/dim mice led to failure to repress ISG genes resulting in excessive necroptosis induction by TNF. Our findings support a critical interplay between gut microbiota, interferons, necroptosis and GR in both the basal response to acute inflammatory challenges and in the pharmacological intervention by GCs.

2018-04-26 | GSE113691 | GEO

RNA-Seq in LPS and Dex+LPS treated bone marrow-derived macrophages

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Glucocorticoid receptor (GR) binding in primary macrophages isolated from WT and GRdim mice

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Glucocorticoid receptor (GR) binding in primary macrophages isolated from WT and GRdim mice

Project description:We report ChIP-seq data for GR in bone marrow-derived primary macrophages isolated from WT and GRdim mice.

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Project description:We mapped the genome wide binding profile of the chromatin remodeller BRG1 in wild type bone marrow derived macrophages (BMDMs) after 3h LPS and LPS plus Dex treatment by ChIPseq. Additionally, we profiled the GR cistrome in Dex + LPS-treated BMDMs after 3h treatment by ChIPseq.

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Essential functions of the Glucocorticoid Receptor require direct DNA binding [RNA-seq]

Project description:We performed RNA sequencing in Mouse Embryonic Fibroblasts (MEFs) of GR wild-type and GR Zn. Cells were treated with: vehicle (EtOH), Dexamethasone (Dex), Lipopolysaccharide (LPS) or Dex+LPS. We show that GR Zn does not regulate any GR target gene

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Characterization of Glucocorticoid Receptor (GR) in Mouse Liver

Project description:We proposed an experiment that determines liver gene regulation profiles in GRLKO. By comparison to the wide type C57BL/6 mouse, we determined the contribution of GR on liver gene expression either at basal level or after Dexamethasone (DEX) injection.

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