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

ABSTRACT: 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.

ORGANISM(S): Ovis aries

PROVIDER: GSE53048 | GEO | 2014/08/07

SECONDARY ACCESSION(S): PRJNA230749

REPOSITORIES: GEO

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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

Campylobacter concisus Impairs sodium absorption in colonic epithelium via ENaC dysfunction and claudin-8 disruption

Project description:The study aimed to characterize C. concisus effects on ENaC using the HT-29/B6-GR/MR cell model.

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Transcription profiling of cortical collecting duct/connecting nephron tissue from mice treated with aldosterone, canrenoate vs. controls to identify gene products regulated by aldosterone in target cells

Project description:The mineralocorticoid hormone aldosterone controls sodium reabsorption and blood pressure largely by regulating the cell-surface expression and function of the epithelial sodium channel ENaC in target kidney tubules. Part of the stimulatory effect of aldosterone on ENaC is mediated by the induction of SGK1, a kinase that interferes with the ubiquitylation of ENaC by ubiquitin-protein ligase Nedd4-2. We performed a microarray study in order to investigate which other gene products are rapidly regulated by aldosterone in target cells that participate to the control of Na+ reabsorption and K+ secretion.

2007-03-07 | E-TABM-229 | biostudies-arrayexpress

Transcription profiling of rat neonatal cardiomyocytes treated with corticosteroid

Project description:Recent studies have highlighted the role of adrenal corticosteroid signaling in cardiac physiology and pathophysiology. It is known that glucocorticoids and aldosterone are able to bind glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), and these ligand-receptor interactions are redundant. Therefore, it has been impossible to delineate how these nuclear receptors couple with corticosteroid ligands and differentially regulate gene expression for operation of their distinct functions in the heart. Here, to particularly define the role of GR, we applied ligand-based approach involving GR-specific agonist cortivazol (CVZ) and GR antagonist RU486, and performed microarray analysis using rat neonatal cardiomyocytes. We indicated that glucocorticoids appear to be a major determinant of GR-mediated gene expression when compared with aldosterone. Moreover, expression profiles of these genes highlighted numerous roles of glucocorticoids in various aspects of cardiac physiology. Experiment Overall Design: We analyzed gene expression changes after exposure of cells to corticosterone (COR), aldosterone (ALD), and cortivazol (CVZ) in the absence or presence of GR antagonist RU486. Since our preliminary experiments using several cell lines showed that expression of many GR target genes was induced by glucocorticoids in 3 h and to avoid secondary effects of the products of GR-regulated genes, we in the present study set the time periods of exposure to these ligands as 3 h. DNA microarray experiments were performed twice with the same protocol except for RU486 treatment.

2009-05-11 | E-GEOD-12752 | biostudies-arrayexpress

Expression data from mDCT cell-line over-expressing hMR

Project description:Target gene of mineralocorticoid receptor (MR) is comparatively unknown, although distal convoluted tubule (DCT) expresses MR in in vivo. We used microarray and immortalized murine DCT cell-line overexpressing human MR with treatment of aldosterone to elucidate target genes of MR in DCT. mDCT overexpresses human MR by lipofection and is treated for 3 hours with ethanol (g1), or 10^-9 M aldosterone (g2), or 10^-7 M aldosterone (g3), or 10^-7 M aldosterone with pretreatment of 5 x 10^-6 M spironolactone (g4) for 2 hours.

2013-11-23 | E-GEOD-52686 | biostudies-arrayexpress

Gene expression data from corticosteroid-treated neonatal rat cardiomyocytes

2009-05-01 | GSE12752 | 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

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

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.

2010-08-12 | GSE23566 | GEO

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

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