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Mus musculus

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

PROVIDER: PRJNA256173 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1525215.fastq.gz	Fastqsanger.gz
	SRR1525216.fastq.gz	Fastqsanger.gz
	SRR1525217.fastq.gz	Fastqsanger.gz

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Similar Datasets

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. Examination of GR binding in WT and GRdim mice on a genome-wide scale

2015-04-14 | E-GEOD-59764 | biostudies-arrayexpress

Prednisolone-induced differential gene expression in liver of mice carrying the wild type or a dimerization-defective glucocorticoid receptor

Project description:Glucocorticoids control expression of a large number of genes after binding to the glucocorticoid receptor (GR). Transcription may be regulated either by binding of the GR dimer to DNA regulatory elements or by protein-protein interactions of GR monomers with other transcription factors. Although the type of regulation for a number of individual target genes is known, the relative contribution of both mechanisms to the regulation of the entire transcriptional program remains elusive. To study the importance of GR dimerization in regulation of gene expression, we performed gene expression profiling in liver of prednisolone-treated wild type (WT) and genetically engineered mice that have lost the ability to form GR-dimers (GRdim). Mice carrying a wild type (WT) glucocorticoid receptor or a dimerization-defective glucocorticoid receptor (GRdim) were treated subcutaneous with vehicle or prednisolone (1mg/kg) and sacrificed 150 minutes later. From the livers of these mice total RNA was extracted, processed and hybridized on Affymetrix microarrays. In total 24 mice (6 vehicle-treated WT mice, 6 prednisolone-treated WT mice, 6 vehicle-treated GRdim mice and 6 prednisolone-treated GRdim mice) were included in the study.

2010-06-08 | E-GEOD-21048 | biostudies-arrayexpress

Genome wide binding of glucocorticoid receptor in dexamethasone treated mouse bone marrow derived macrophages

Project description:Macrophages are amongst the major targets of glucocorticoids (GC) as therapeutic anti-inflammatory agents. Here we show that GC treatment of mouse and human macrophages initiates a cascade of induced gene expression including many anti-inflammatory genes. Inducible binding of the glucocorticoid receptor (GR) was detected at candidate enhancers in the vicinity of induced genes in both species and this was strongly associated with canonical GR binding motifs. However, the sets of inducible genes, the candidate enhancers, and the GR motifs within them, were highly-divergent between the two species. Mouse bone marrow derived macrophages were generated from two male 10 week old C57BL/6 mice, treated with dexamethsone 100nM or vehicle and glucocorticoid receptor bound DNA extracted by chromatin immunoprecipitation

2015-12-17 | E-GEOD-61877 | biostudies-arrayexpress

Glucocorticoid Regulated Transcriptome in Wild-type and GR-C3 Knockin Mouse Embryonic Fibroblasts

Project description:Glucocorticoids are primary stress hormones and their synthetic derivatives are widely used clinically. The therapeutic efficacy of these steroids is limited by severe side effects and glucocorticoid resistance. Multiple glucocorticoid receptor (GR) isoforms are produced by alternative translation initiation; however, the role individual isoforms play in controlling tissue-specific responses to glucocorticoids in vivo is unknown. We have generated knockin mice that exclusively express the most active receptor isoform, GR-C3. The GR-C3 knockin mice die at birth due to respiratory distress but can be completely rescued by antenatal glucocorticoid administration. To evaluate the GR-C3 transcriptome, we prepared mouse embryonic fibroblasts (MEFs) from E12.5 wild-type (WT) and GR-C3 knockin embryos and treated the cells with vehicle or the synthetic glucocorticoid Dexamethasone (Dex) for 6 hours. The GR-C3 isoform was found to have a markedly different gene-regulatory profile than GR in WT MEFs.

2018-04-23 | GSE103675 | GEO

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.

2015-04-14 | GSE59764 | GEO

Inflammatory Gene Changes in Spleens from WT and Rescued GR-C3 Knockin Mice Treated with LPS

Project description:Glucocorticoids are primary stress hormones and their synthetic derivatives are widely used clinically. The therapeutic efficacy of these steroids is limited by severe side effects and glucocorticoid resistance. Multiple glucocorticoid receptor (GR) isoforms are produced by alternative translation initiation; however, the role individual isoforms play in controlling tissue-specific responses to glucocorticoids in vivo is unknown. We have generated knockin mice that exclusively express the most active receptor isoform, GR-C3. The GR-C3 knockin mice die at birth due to respiratory distress but can be completely rescued by antenatal glucocorticoid administration. Rescued GR-C3 mice exhibited alterations in circadian rhythm in a sexually dimorphic manner and in sensitivity to lipopolysaccharide (LPS)-induced endotoxemia. To evaluate the ability of glucocorticoids to protect against LPS-induced inflammation, we measured gene expression in spleens from WT and rescued GR-C3 knockin mice that had been treated with vehicle or LPS for 3 and 24 hours. The GR-C3 isoform was found to be deficient in its ability to repress a large cohort of immune and inflammatory genes.

2018-05-08 | GSE103721 | GEO

Creation of an anti-inflammatory GR cistrome by TLR4 signaling

Project description:An unresolved molecular paradox is how the glucocorticoid receptor (GR) activates some genes while potently repressing others. We carried out genome-wide localization and expression profiling experiments in primary bone marrow-derived mouse macrophages treated with Dexamethasone in the presence or absence of LPS. Unexpectedly, we find that the anti-inflammatory GR cistrome, which is principally composed of 'canonical' GREs colocalizing with NFkB and AP-1 co-enriched with the myeloid lineage factors C/EBP and Pu.1, is shaped by TLR4-directed chromatin dynamics, suggesting that context rather than sequence may be a critical determinant of function. Identification of GR, cJun, NFkB(p65) binding sites in primary bone-marrow derived macrophages unstimulated and LPS-stimulated (3hrs) that were untreated or pre-treated with Dexamethasone for 16 hrs

2012-12-04 | E-GEOD-31796 | biostudies-arrayexpress

The Signature of Glucocorticoid Receptor -Dependent Hypertrophic Transcriptome in Cardiomyocytes [ChIP-Seq]

Project description:We examined Glucocorticoid receptor binding sites in isolated neonatal cardiomyocytes treated with Dexamethasone (100nM) for 1hr or Ethanol using GR-ChIP-Seq.

2019-08-20 | GSE114616 | GEO

Changes in nascent transcripts upon glucocorticoid stimulation in macrophages

Project description:Glucocorticoids are widely prescribed anti-inflammatory drugs with tissue-specific effects. Beneficial anti-inflammatory effects are caused in cells of the immune system whereas metabolic adverse effects of glucocorticoid therapy are seen in metabolic tissues such as liver. The glucocorticoid receptor (GR), a nuclear receptor targeted by glucocorticoids, bind its DNA response elements upon ligand exposure in a tissue-specific manner. Tissue-specific GR binding patterns depend on the access of its binding sites, which determines the tissue-specific glucocorticoid response. Here, we investigated this response by nascent RNAseq in murine bone marrow-derived macrophages (BMDMs) after stimulation with lipopolysaccharide (LPS) and dexamethasone (Dex). After labelling newly synthesized transcripts with 4-thiouracile (4sU), we identified macrophage-specific non-coding transcripts expressed at intergenic GR binding sites. Those transcripts are regulated by the GR and correlate with its anti-inflammatory function in macrophages. Those findings add another layer to the mechanisms underpinning GR's tissue-specific gene regulation and represent potential drug targets in anti-inflammatory therapy and/or management of adverse effects in glucocorticoid therapy.

2021-12-31 | GSE186629 | GEO

Divergent transcriptional activation by glucocorticoids in mouse and human macrophages is the result of gain and loss of enhancers

Project description:Macrophages are amongst the major targets of glucocorticoids (GC) as therapeutic anti-inflammatory agents. Here we show that GC treatment of mouse and human macrophages initiates a cascade of induced gene expression including many anti-inflammatory genes. Inducible binding of the glucocorticoid receptor (GR) was detected at candidate enhancers in the vicinity of induced genes in both species and this was strongly associated with canonical GR binding motifs. However, the sets of inducible genes, the candidate enhancers, and the GR motifs within them, were highly-divergent between the two species. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-17 | E-GEOD-61881 | biostudies-arrayexpress

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