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When glucocorticoid receptor meets the mineralocorticoid receptor in human cells

ABSTRACT: When glucocorticoid receptor meets the mineralocorticoid receptor in human cells

PROVIDER: PRJNA1149651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30294517.fastq.gz	Fastqsanger.gz
	SRR30294518.fastq.gz	Fastqsanger.gz
	SRR30294519.fastq.gz	Fastqsanger.gz
	SRR30294520.fastq.gz	Fastqsanger.gz
	SRR30294521.fastq.gz	Fastqsanger.gz

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When glucocorticoid receptor meets the mineralocorticoid receptor in human cells

Project description:Glucocorticoids are widely used to treat a variety of inflammatory diseases. Mechanistically glucocorticoid ligands induce glucocorticoid receptor (GR) homodimerization and regulation of gene expression. Here we show that GR and mineralocorticoid receptor (MR) form molecular complexes with distinct transcriptional responses that alter the biological roles of GR. MR inhibited GR interaction with genomic DNA and diminished glucocorticoid-regulated gene expression as well as suppressed cell apoptosis induced by GR signaling.

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Effect of Mineralocorticoid Receptor deletion on glucocorticoid signalling in the macropahge

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Effect of Mineralocorticoid Receptor deletion on glucocorticoid signalling in the macropahge

Project description:Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone- independent mechanisms. We used affymetrix to characterize the effect of Mineralocorticoid Receptor deletion on macrophage transcriptional profile, and identify its requirement in normal glucocorticoid signalling. We isolated mouse peritoneal macrophages from Myeloid MRKO mice and Floxed Controls, cultured in the presence or absence of corticosterone. RNA was extracted for Affymetrix cDNA hybridization. Each sample was pooled from experiments performed in triplicate.

2010-07-30 | E-GEOD-23308 | biostudies-arrayexpress

Mineralocorticoid receptor co-expression effect on ligand-induced glucocorticoid receptor interaction with the genome in human cell line

Project description:Our previous results observed glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) physical and functional interactions. RNAseq study (GSE163506) revealed that MR blunted GR ligand-dependent gene regulation in human cell lines. In the current study, we developed U-2 OS cell line-derived cells constitutively expressing GR or MR plus GR. Then, we compared GR – genome interaction before and after dexamethasone treatment.

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The glucocorticoid receptor potentiates aldosterone-induced transcription by the mineralocorticoid receptor

Project description:The glucocorticoid receptor potentiates aldosterone-induced transcription by the mineralocorticoid receptor

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Crosstalk between the glucocorticoid and mineralocorticoid receptor boosts glucocorticoid-induced killing of multiple myeloma cells

Project description:The glucocorticoid receptor (GR) is a crucial drug target in multiple myeloma as its activation with glucocorticoids effectively triggers myeloma cell death. However, as high-dose glucocorticoids are also associated with deleterious side effects, novel approaches are urgently needed to improve GR’s action in myeloma. Here we reveal a functional crosstalk between GR and the mineralocorticoid receptor (MR) that culminates in improved myeloma cell killing. We show that the GR agonist Dexamethasone (Dex) downregulates MR levels in a GR-dependent way in myeloma cells. Co-treatment of Dex with the MR antagonist Spironolactone (Spi) enhances Dex-induced cell killing in primary, newly diagnosed GC-sensitive myeloma cells, while in a relapsed GC-resistant setting, Spi alone induces distinct myeloma cell killing. On a mechanistic level, we find that a GR-MR crosstalk is arising from an endogenous interaction between GR and MR in myeloma cells. Quantitative dimerization assays show that Spi reduces Dex-induced GR-MR heterodimerization and completely abolishes Dex-induced MR MR homodimerization but leaves GR-GR homodimerization intact. Unbiased transcriptomics further reveals that c-myc and many of its target genes are downregulated most by Dex and Spi combined, while proteomics analyses identify that several metabolic hallmarks are modulated most by this combination treatment. Finally, we identified a subset of Dex+Spi downregulated genes and proteins that may predict prognosis in the CoMMpass patient cohort. Our study demonstrates that GR-MR crosstalk is therapeutically relevant in myeloma as it provides novel strategies towards glucocorticoid-based dose-reduction.

2023-10-24 | PXD043635 | Pride

Knockdown of mineralocorticoid receptor or glucocorticoid receptor on human endometrial stromal cells and decidualization

Project description:To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.

2012-11-28 | GSE42538 | GEO

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Project description:Purpose: To compare the binding profiles of mineralocorticoid and glucocorticoid receptors after corticosterone treatment in neuroblastoma cells. Methods: Tagged glucocorticoid receptors (eGFP-rat GR) and mineralocorticoid receptors (mCherry-rat MR) were transiently transfected into Neuro2A mouse neuroblastoma cells and treated with (i) vehicle, (ii) corticosterone 100 nM for 20 mins and (iii) corticosterone 100 nM for 20 mins followed by media repacement twice and 40 mins further incubation in charcoal-stripped serum media. ChIP-nexus samples were prepared in triplicate for deep sequencing using Illumina NextSeq, as well as control samples taken from cell lysates before immunoprecipitation. Sequence data was analyzed and processed for the identification of enriched binding sites, using MACS2, and for the characteristic staggered ChIP-nexus borders, using the MACE pipeline (Wang et al., 2014). Results: Corticosterone-sensitive glucocorticoid receptor (GR) binding sites and mineralocorticoid receptor (MR) binding sites showed considerable overlap, by MACS2 analysis. GR and MR binding sites were highly similar showing recruitment to the same DNA sites, by MACE analysis (Wang et al., 2014). Further analyses showed GR could tether MR to the DNA by GR in a functional manner such that gene expression could be altered by the presence of tethered MR. Conclusions: MR can be recruited to DNA-binding sites by GR, even in the absence of MR DNA-binding. MR can interact in multiple modes at genomic DNA binding sites.

2019-03-15 | GSE115417 | GEO

Exploiting crosstalk between glucocorticoid and mineralocorticoid receptors enhances glucocorticoid-induced killing of multiple myeloma cells

Project description:Long-term glucocorticoid treatment in multiple myeloma is hampered by deleterious side effects. Glucocorticoids bind to the glucocorticoid receptor (GR), which is a crucial drug target because its activation triggers myeloma cell death. The mineralocorticoid receptor (MR) is a closely related nuclear receptor but its impact on glucocorticoid responsiveness in myeloma is unknown. Here we reveal a functional crosstalk between GR and MR that culminates in improved myeloma cell killing. We show that the GR agonist Dexamethasone (Dex) downregulates MR levels in a GR-dependent way in myeloma cells. Co-treatment of Dex with the MR antagonist Spironolactone enhances Dex-induced cell killing in (primary) myeloma cells. The crosstalk is further evidenced by an endogenous interaction between GR and MR in myeloma cells that is ligand-inducible and by a distinctive gene expression profile. Our study demonstrates that GR-MR crosstalk is therapeutically relevant in myeloma and presents a glucocorticoid-based dose-reduction strategy that could diminish glucocorticoid-related side effects in patients.

2023-08-23 | GSE200313 | GEO

Knockdown of mineralocorticoid receptor or glucocorticoid receptor on human endometrial stromal cells and decidualization

Project description:To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells. Genome-wide microarray analysis was performed on primary cultures established from 4 different patients. Stromal cell cultures were subjected to either GR or MR siRNA knockdown or control non-targeting siRNA then decidualized for four days before harvesting and RNA extraction for microarray analysis.

2012-11-28 | E-GEOD-42538 | biostudies-arrayexpress

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