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Aldosterone-inducible genes in mineralocorticoid receptor expressed human endothelial cell lines

ABSTRACT: To elucidate the aldosterone-regulated genes in vascular endothelial cells, we developed human endothelial cell line (EAhy926) stably expressing human mineralocorticoid receptor by retroviral system (MR-EAhy). Then gene expression profile of MR-EAhy stimulated with or without aldosterone was compared using DNA microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28009 | GEO | 2011/03/18

SECONDARY ACCESSION(S): PRJNA137983

REPOSITORIES: GEO

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Aldosterone-inducible genes in mineralocorticoid receptor expressed human endothelial cell lines

Project description:To elucidate the aldosterone-regulated genes in vascular endothelial cells, we developed human endothelial cell line (EAhy926) stably expressing human mineralocorticoid receptor by retroviral system (MR-EAhy). Then gene expression profile of MR-EAhy stimulated with or without aldosterone was compared using DNA microarray analysis. MR-EAhy were serum-deprived for 24h with 0.2% dextran-coated charcoal-treated FBS, and then stimulated with or without aldosterone (10-9 M) for 6 hr. Then cells were harvested for RNA extraction.

2011-03-18 | E-GEOD-28009 | biostudies-arrayexpress

Cistrome of the Aldosterone-activated Mineralocorticoid Receptor in Human Renal Cells

Project description:Aldosterone, the main mineralocorticoid hormone in Humans, has a major role in maintaining the hemo-electrolytique homeostasis, by acting in the distal part of nephron. This steroid hormone mainly acts through its binding to a ligand-induced transcription factor, the mineralocorticoid receptor (MR). MR binds to specific genomic sequences, where it recruits transcriptional coregulators, to activate or repress target gene transcription. The aim of this work was to access the whole aldosterone-dependand MR target genes, by comparing sequenced data from aldosterone or vehicle-treated samples. Anti-MR ChIP-seq in Human Kidney GFP-hMR cells treated with vehicle or Aldosterone.

2015-06-12 | E-GEOD-69777 | biostudies-arrayexpress

Cistrome of the Aldosterone-activated Mineralocorticoid Receptor in Human Renal Cells

2015-06-12 | GSE69777 | GEO

Cardiac aldosterone and corticosterone regulated genes in mice with cardiomyocytes targeted mineralocorticoid receptor overexpression (MR-Cardio mice) and their controls (Ctrl mice)

Project description:Inappropriate mineralocorticoid receptor (MR) activation is involved in cardiac diseases. MR binds aldosterone, but also glucocorticoids; the identity of the ligand responsible for the deleterious effects of cardiac MR activation is still unclear. Mice overexpressing MR in cardiomyocytes (MR-Cardio) and their controls (Ctrl) were treated for 7 days with aldosterone or corticosterone and a whole genome microarray analysis was performed.

2017-09-01 | GSE33022 | GEO

Cardiac aldosterone regulated genes in mice with cardiomyocytes targeted mineralocorticoid receptor overexpression (MR-Cardio mice) and their controls (Ctrl mice)

Project description:Inappropriate mineralocorticoid receptor (MR) activation is involved in cardiac diseases. The mechanisms are still unclears. Mice overexpressing MR in cardiomyocytes (MR-Cardio) and their controls (Ctrl) were treated for 7 days with aldosterone and a whole genome microarray analysis was performed.

2017-09-01 | GSE34049 | GEO

Aldosterone-Regulated Expression Data in Mouse Aorta

2010-08-12 | GSE23566 | GEO

Effect of Mineralocorticoid Receptor deletion on glucocorticoid signalling in the macropahge

2010-07-30 | GSE23308 | GEO

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 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

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

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