Dexamethasone stimulated gene expression in peripheral blood
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE64930 | GEO | 2015/11/03
SECONDARY ACCESSION(S): PRJNA272522
REPOSITORIES: GEO
Similar Datasets
Project description:Whole genome gene expression data (baseline and following GR-stimulation with 1.5 mg dexamethasone p.o.) were analysed to identify glucocorticoid receptor (GR)-mediated changes in gene expression. A Dexamethasone Suppression Test was performed in 297 subjects. Baseline and stimulated (3 hours after 1.5 mg dexamethasone p.o.) whole blood samples were analyzed using Illumina Human HT-12 v3 and v4 arrays.
2015-11-03 | E-GEOD-64930 | biostudies-arrayexpress
Project description:Whole-genome DNA methylation (baseline and following GR-stimulation with 1.5 mg dexamethasone p.o.) were analysed to identify glucocorticoid receptor (GR)-mediated changes in DNA methylation. Lifetime stress accelerates epigenetic aging.
2015-11-03 | GSE74414 | GEO
Project description:Whole-genome DNA methylation (baseline and following GR-stimulation with 1.5 mg dexamethasone p.o.) were analysed to identify glucocorticoid receptor (GR)-mediated changes in DNA methylation. Lifetime stress accelerates epigenetic aging. DNA methylation was assessed in whole blood at baseline and 3 hours after stimulation with the selective GR agonist dexamethasone (1.5 mg p.o.). Blood was collected in EDTA vacuum tubes prior to extraction. DNA methylation was interrogated for each sample using the HumanMethylation450 BeadChip (Illumina). Supplementary files 'GSE74414_unmethylated_signals_353_CpG.txt', 'GSE74414_methylated_signals_353_CpG.txt', and 'GSE74414_detection.p.values_353_CpG.txt' include the raw data for the 353 CpGs used in the analysis in the associated manuscript. Supplementary file 'GSE74414_beta_values_353_CpG.txt' includes the processed data for the 353 CpGs used in the analysis in the associated manuscript. The raw and processed data for the remaining features included in Platform GPL13534 are embargoed.
2015-11-03 | E-GEOD-74414 | biostudies-arrayexpress
Project description:Analysis of dexamethasone-stimulated A549 lung adenocarcinoma epithelial cells treated with a glucocorticoid response (GR) element (GRE) specific DNA binding polyamide. Polyamide designed to target the sequence 5'-WGWWCW-3' and disrupt GR-mediated gene expression. Effects of the GR antagonist mifepristone also examined.
2009-09-01 | GSE17307 | GEO
Project description:Glucocorticoids are critical components of combination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL). However, the signaling pathways regulating apoptosis in glucocorticoid-treated lymphoid cells remain unclear. In this study, pediatric ALL patient-derived xenograft inherently sensitive to glucocorticoids were exposed to dexamethasone in vivo. Whole-genome GR binding sites and histone acetylation status were detected using chromatin immunoprecipitation sequencing analyses. This provided a global understanding of dexamethasone-induced DNA modulations in ALL cells in vivo, which is likely to be important in the understanding of mechanisms of glucocorticoid response in lymphoid malignancies. One xenograft (ALL-54) was derived from a patient of dexamethasone-good responder. The xenograft was innoculated into 2 NOD/SCID mice, and treated with dexamethasone (15 mg/kg) or vehicle control. Binding of glucocorticoid receptor (GR), histone acetylation and IgG control in spleen-harvest xenograft samples were detected using ChIP-seq.
2014-12-18 | E-GEOD-58266 | biostudies-arrayexpress
Project description:Analysis of dexamethasone-stimulated A549 lung adenocarcinoma epithelial cells treated with a glucocorticoid response (GR) element (GRE) specific DNA binding polyamide. Polyamide designed to target the sequence 5'-WGWWCW-3' and disrupt GR-mediated gene expression. Effects of the GR antagonist mifepristone also examined. Experiment Overall Design: A549 cells were treated with compounds for 48 hours before RNA extraction and hybridization on Affymetrix microarrays.
2009-09-13 | E-GEOD-17307 | biostudies-arrayexpress
Project description:The treatment of advanced prostate cancer has been transformed by novel antiandrogen therapies such as enzalutamide. We identified glucocorticoid receptor (GR) activity as modulator of enzalutamite sensitivity in the VCaP prostate cancer cell line. The GR agonist dexamethasone was sufficient to confer enzalutamide resistance whereas a GR antagonist restored sensitivity. These expression profiling data demonstrate that GR transcriptional activity overlaps with that of AR in the VCAP model.
2013-12-27 | GSE51872 | GEO
Project description:The glucocorticoid receptor (GR) is a transcription factor that localizes to the nucleus and reuglates gene expression upon binding of a glucocorticoid ligand such as dexamethasone. We perform nascent transcriptional profiling of C7 ALL cells following treatment with dexamethasone to evaluate the immediate transcriptional effects of GR. We find 51 dynamic genes (46 activated, 5 repressed) after 1 hour treatment and 141 dynamic genes (70 activated and 71 repressed) after 4 hour treatment. We input RNA polymerase density in pause and gene body regions into a mathematical model designed to quantify rate changes of individual transcriptional steps. We find that dexamethasone treatment primarily activates genes by inducing pause release rate.
2022-12-04 | GSE219041 | GEO
Project description:GLUCOCORTICOIDS are steroid hormones that strongly influence intermediary carbohydrate metabolism by increasing the transcription rate of glucose-6-phosphatase (G6Pase) a key enzyme of gluconeogenesis, and suppress the immune system which makes them one of the most important therapeutic agents in the treatment of allergic, autoimmune and inflammatory diseases. The biologic actions of circulating glucocorticoids are transmitted to the cells nucleus by the glucocorticoid receptor (GR). The nuclear liver X receptors (LXRs) bind to cholesterol metabolites, heterodimerize with the retinoid X receptor (RXR), and regulate the cholesterol turnover, the hepatic glucose metabolism by decreasing the expression of G6Pase, and repress a set of inflammatory genes in immune cells. The aim of this study is to evaluate the crosstalk between the GR- and LXR-mediated signaling systems. Transient transfection-based reporter assays and gene silencing methods using siRNAs for LXRs showed that overexpression/ligand (GW3965) activation of LXRs/RXRs repressed GR-stimulated transactivation of certain glucocorticoid response element (GRE)-driven promoters in a gene-specific fashion. Activation of LXRs by GW3965 attenuated dexamethasone-stimulated elevation of circulating glucose in rats and suppressed dexamethasone-induced mRNA expression of hepatic glucose-6-phosphatase (G6Pase) in rats, mice and human hepatoma HepG2 cells. In microarray transcriptomic analysis of rat liver, GW3965 differentially regulated glucocorticoid-induced transcriptional activity of about 15% of endogenous glucocorticoid-responsive genes. Mechanistically, and in vitro chromatin immunoprecipitation assay, we found that LXRα/RXRα bound GREs and inhibited GR binding to these DNA sequences in a gene-specific fashion. These novel results were further confirmed in in vivo binding assays, and in gel mobility shift assays, where recombinant LXRα/RXRα proteins were used to examine their interaction with classic or G6Pase GREs. We propose that administration of LXR agonists may be beneficial in glucocorticoid treatment- or stress-associated dysmetabolic states by directly attenuating the transcriptional activity of the GR on glucose and/or lipid metabolism. 4 Sprague-Dawley rats (180-200g) were orally gavaged for three days with GW3965 prepared in 1% Tween 80, 0.5% hydroxypropyl methylcellulose, 20 mM Na2HPO4 and 20 mM NaH2PO4 (50 mg/kg animal). Another set of animals were also orally gavaged with the same volume of the vehicle control (1% Tween 80, 0.5% hydroxypropyl methylcellulose, 20 mM Na2HPO4 and 20 mM NaH2PO4). On the third day, GW3965 or its vehicle control was administered first to the animals followed by an intra-muscularly injection of dexamethasone (1.5 mg/kg) or physiologic saline in two animals from each group. Twenty-four hours after the injection, levels of blood glucose were measured in these rats using the Freestyle GlucoMeter (Abbott Laboratories, Abbott Park, IL) by sampling blood from their tails. The animals were then euthanized using CO2, and their livers were harvested for extraction and purification of total RNA and proteins. Five μg of total RNA purified from rat livers was used for producing probes with the One-Cycle Target Labeling and Control Reagents Kit (Affymetrix, Inc., Santa Clara, CA). [Rat230_2] Affymetrix Rat Genome 230 2.0 Arrays (Affymetrix Inc.) were then labeled with the prepared probes.
2012-04-01 | E-GEOD-29912 | biostudies-arrayexpress
Project description:The RNA binding ability of the glucocorticoid receptor (GR) remains an understudied area of GR regulation. Through in vitro binding assays, we identified hairpin RNAs as GR's preferred binding motif. To study how GR-bound RNAs change with dexamethasone treatment, we first generated stable U2OS cells expressing wild-type GR-HaloTag. We then treated the cells with dexamethsone every hour over three hours, UV crosslinked, harvested, and pulled down GR using a specific and covalently-bound HaloTag ligand. GR-bound RNAs were then isolated, library prepped, and sequenced.
2022-12-17 | GSE217888 | GEO