Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from human primary skeletal muscle myotubes treated with aldosterone, spironolactone, eplerenone, mifepristone, prednisolone or vehicle

ABSTRACT: To define the direct gene expression changes in normal human skeletal muscle with mineralocorticoid and glucocorticoid receptor agonist and antagonist treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE84990 | GEO | 2017/05/05

SECONDARY ACCESSION(S): PRJNA335846

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from human primary skeletal muscle myotubes treated with aldosterone, spironolactone, or vehicle.

2015-07-14 | GSE70822 | GEO

Expression data from human primary skeletal muscle myotubes treated with aldosterone, spironolactone, or vehicle.

Project description:To test for a function effect of mineralocorticoid receptor modulation in skeletal muscle, global gene expression analysis was conducted on human myltubes treated with a mineralocorticoid receptor agonist or antagonist. 9 total samples were analyzed. 3 biological replicates for each of the following treatment groups were included: 1) aldosterone; 2) spironolactone; 3) vehicle (ethanol). Pairwise comparison between groups were carried out and a fold-change ≥2 were selected.

2015-07-14 | E-GEOD-70822 | biostudies-arrayexpress

Expression data from human primary skeletal muscle myotubes treated with aldosterone alone or co-incubated with aldosterone plus spironolactone, eplerenone, or mifepristone

Project description:To uncover whether aldosterone induces gene expression changes through mineralocorticoid or glucocorticoid receptors and determine if eplerenone and spironolactone could block aldosterone induced gene expression to the same extent

2017-05-05 | GSE84991 | GEO

Differential antagonistic effects of finerenone and spironolactone on the aldosterone transcriptome in human kidney cells.

Project description:Aldosterone, the main mineralocorticoid hormone in humans, controls, via gene transregulation, various renal functions including water and sodium reabsorption and potassium excretion. Dysregulations in the aldosterone signaling pathway lead to renal dysfunctions, including chronic kidney disease and renal fibrosis, that can be prevented or treated with mineralocorticoid receptor antagonists (MRAs). To understand the global effects of aldosterone on the human renal transcriptome, and how it is antagonized by the MRAs spironolactone and finerenone, we used RNA-sequencing on a human kidney cells HK-GFP-hMR. Our data provide the first complete transcriptome for aldosterone on a human renal cell line and support at the RNA level the benefit of finerenone for the treatment of kidney injury and fibrosis.

2022-05-09 | GSE151321 | GEO

Comparison of the in vivo transcriptome of the myometrium exposed to mifepristone vs vehicle

Project description:Circulating progesterone (P4) levels decline before the onset of parturition in most animals, but not in humans. This has led to the suggestion that there is functional withdrawal of P4 action at the myometrial level prior to labor onset. However, to date, no evidence of a loss of P4 function has been provided. Mifepristone is a mixed progesterone and glucocorticoid receptor antagonist that is frequently used to induce human labor. However, its effect on the myometrial tissue transcriptome hs not been determined. In this study, we aimed to identify the effects of mifepristone treatment on the pregnant myometrium at term in order to better understand the possible mechanisms underlying the loss of P4 function in human labor.

2019-02-01 | GSE77831 | 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

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.

2010-07-30 | GSE23308 | GEO

Effect of 48 h aldosterone treatment on late-gestation fetal lung

Project description:The late-gestation fetal lung has relatively high levels of expression of the mineralocorticoid receptor (MR) as well as the glucocorticoid receptor (GR), suggesting that endogenous corticosteroids may act in the lung through binding at MR as well as GR. This study was designed to determine the effects of physiologically relevant increases in steroids on MR and GR in the late-gestation lung. The GR agonist, betamethasone, the MR agonist, aldosterone, or both agonists were infused intravenously for 48 hours in ovine fetuses of approximately 130 days gestation. Effects on airway pressures during stepwise inflation of the in situ lung, expression of ENaC and Na,K ATPase, and elastin and collagen content were determined at the end of the infusions. We found that aldosterone significantly reduced the initial airway pressures measured in situ during inflation. This effect did not occur with betamethasone alone or in combination with aldosterone. Conversely, betamethasone, but not aldosterone, significantly increased expression of the epithelial sodium channel (ENaC) subunit mRNAs, and collagen and elastin content in the lungs. Aldosterone altered novel gene pathways in the fetal lung, suggesting effects on lung compliance via genes which influence immune pathways and lung stiffness. The results are consistent with corticosteroid-induced fluid reabsorption at birth through GR rather than MR, but suggest that MR contributes effects facilitating lung inflation with the first breaths via nonclassical mechanisms. 4 sets of twin sheep fetuses at approximately 130d gestation (term is 147d) were used. One twin was infused with 0.2 mg aldosterone for 48 h, the other received vehicle.

2014-08-07 | E-GEOD-53048 | biostudies-arrayexpress

Aldosterone-Regulated Expression Data in Mouse Aorta

Project description:The steroid hormone aldosterone plays a role in vascular function and disease. Aldosterone activates the mineralocorticoid receptor (MR), a ligand-activated transcription factor. MR have been found to be expressed in vascular cells and vessels. We used microarrays to identify the global programme of gene expression changes in mouse aortas treated with vehicle (DMSO) or aldosterone. Wild type C57Bl6 male mice were treated with spironolactone (20 mg/kg/day, an MR antagonist) for 5 days by Sub-cutaneous pellet to suppress basal MR-mediated gene expression. Aortas were then harvested and treated ex vivo in organ culture with vehicle or 100 nM aldosterone for 2, 4, or 8 hours. Three aortas were pooled for each timepoint and treatment, and three pooled biological replicates were performed.

2010-08-12 | E-GEOD-23566 | biostudies-arrayexpress

Effect of 48 h aldosterone treatment on late-gestation fetal lung

2014-08-07 | GSE53048 | GEO