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Mus musculus

ABSTRACT: Anti-inflammatory Chromatinscape Associated with Clinically Relevant Timing of Glucocorticoid Treatment [DNase-seq]

PROVIDER: PRJNA362229 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5182714.fastq.gz	Fastqsanger.gz
	SRR5182715.fastq.gz	Fastqsanger.gz
	SRR5182716.fastq.gz	Fastqsanger.gz
	SRR5182717.fastq.gz	Fastqsanger.gz
	SRR5182718.fastq.gz	Fastqsanger.gz

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Project description:Anti-inflammatory Chromatinscape Associated with Clinically Relevant Timing of Glucocorticoid Treatment [RNA-Seq]

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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

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Project description:The aim of the experiment was to gain insight into the selective anti-inflammatory action of the glucocorticoid receptor modulator AZD9567 in comparison with the classical synthetic glucocorticoid dexamethasone. To this end, the transcriptional profile of macrophage RAW 264.7 cells treated with dexamethasone or AZD9567 in the presence or absence of inflammatory response (elicited by lipopolysaccharide treatment) was identified.

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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

Anti-inflammatory Chromatinscape Associated with Clinically Relevant Timing of Glucocorticoid Treatment [DNase-seq]

Project description:Despite the widespread use of glucocorticoids (GCs) for treating inflammatory conditions, the underlying mechanisms of their anti-inflammatory effects are not understood. Moreover, the majority of molecular investigations have examined the effects of glucocorticoid receptor (GR) activation prior to inflammatory challenges. However, clinically relevant situations are emulated by a GC intervention initiated in the midst of rampant inflammatory responses. To characterize the effects of a late GC treatment, we performed systematic profiling of macrophage transcriptional and regulatory landscapes with Dexamethasone (Dex) treatment either before or after stimulation by lipopolysaccharide (LPS). GR activation by Dex following LPS stimulation had a similar anti-inflammatory profile in comparison to GR pre-activation, while ameliorating the disruption of metabolic genes. Unexpectedly, the chromatin occupancy pattern of GR is not predictive of the Dex-regulated expression changes and shows little evidence for the widely accepted ‘trans-repression by tethering’ model. Rather, we find that GR activation results in global blockade of NF-κB binding to chromatin. Integrative analyses of gene expression, transcription factor occupancy, and chromatin accessibility data highlight distinct mechanisms through which GR controls inflammatory macrophages: prevention of NF-κB chromatin occupancy and activation of negative regulators such as Nfkbia, Dusp1, Tnfaip3, and Tsc22d3. Our investigation with differentially timed GC treatments reveals molecular mechanisms underlying therapeutic actions of GR for modulating the ‘inflamed epigenome’.

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Anti-inflammatory Chromatinscape Associated with Clinically Relevant Timing of Glucocorticoid Treatment [ChIP-seq]

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