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Mus musculus

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

PROVIDER: PRJNA262583 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1592590_1.fastq.gz	Fastqsanger.gz
	SRR1592590_2.fastq.gz	Fastqsanger.gz
	SRR1592591_1.fastq.gz	Fastqsanger.gz
	SRR1592591_2.fastq.gz	Fastqsanger.gz
	SRR1592592_1.fastq.gz	Fastqsanger.gz

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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

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Homo sapiens

Project description:Genome wide binding of glucocorticoid receptor in dexamethasone treated human monocyte derived macrophages

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Profiling of Polyadenylated RNAs after Brg1/Smarca4 knock-down in murine bone marrow-derived macrophages after LPS or LPS plus Dex stimulation [RNA-seq]

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Effect of FOXO3 on GR Signaling

Project description:To identify cross-talk between the transcription factors, glucocorticoid receptor and FOXO3 after activation of the glucocorticoid receptor with dexamethasone.Bone marrow derived macrophages lacking FOXO3 were exposed to vehicle, dexamethasone, a synthetic glucocorticoid.

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Creation of an anti-inflammatory GR cistrome by TLR4 signaling

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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 NF-κB 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.

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

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2022-06-03 | PXD007793 | Pride

The auophagy receptor SQSTM1/p62 mediates anti-inflammatory actions of the selective NR3C1/glucocorticoid receptor modulator compound A (CpdA) in macrophages

Project description:Glucocorticoids are widely used to treat inflammatory disorders; however, prolonged use of glucocorticoids results in side effects including osteoporosis, diabetes and obesity. Compound A (CpdA), identified as a selective NR3C1/glucocorticoid receptor (nuclear receptor subfamily 3, group C, member 1) modulator, exhibits an inflammation-suppressive effect, largely in the absence of detrimental side effects. To understand the mechanistic differences between the classic glucocorticoid dexamethasone (DEX) and CpdA, we looked for proteins oppositely regulated in bone marrow-derived macrophages using an unbiased proteomics approach. We found that the autophagy receptor SQSTM1 but not NR3C1 mediates the anti-inflammatory action of CpdA. CpdA drives SQSTM1 upregulation by recruiting the NFE2L2 transcription factor to its promoter. In contrast, the classic NR3C1 ligand dexamethasone recruits NR3C1 to the Sqstm1 promoter and other NFE2L2-controlled gene promoters, resulting in gene downregulation. Both DEX and CpdA induce autophagy, with marked different autophagy characteristics and morphology. Suppression of LPS-induced Il6 and Ccl2 genes by CpdA in macrophages is hampered upon Sqstm1 silencing, confirming that SQSTM1 is essential for the anti-inflammatory capacity of CpdA, at least in this cell type. Together, these results demonstrate how off-target mechanisms of selective NR3C1 ligands may contribute to a more efficient anti-inflammatory therapy.

2019-06-11 | PXD012121 | Pride

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