Dexamethasone stimulated gene expression in peripheral blood
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Janine Arloth
PROVIDER: E-GEOD-64930 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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.
2015-11-03 | GSE64930 | 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.
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:While exposure to adverse life events and subsequent dysregulation of the stress hormone response broadly confer risk for depression, the specific molecular mechanisms mediating this risk are poorly understood. Through pharmacologic activation of the stress hormone response in blood cells we demonstrate that common genetic variants in long-range enhancer elements moderate the immediate transcriptome response to stress, and that these genetic differences are associated with increased risk for depression in the context of early adversity. Using imaging genetics we then link these common risk variants with dysregulated amygdala reactivity, an important trigger of the stress hormone response. The transcripts regulated by these risk variants in peripheral blood were also responsive to stress and stress hormone receptor activation in murine brain. Network modeling approaches suggest that these differences in transcriptional activation may mediate stress-related risk for depression by altering a functional gene network related to proteasome degradation and synaptic plasticity. A Dexamethasone Suppression Test was performed in 160 male subjects. Baseline and stimulated (3 hours after 1.5 mg dexamethasone p.o.) whole blood samples were analyzed using Illumina Human HT-12 v3 arrays.
2013-09-01 | E-GEOD-46743 | biostudies-arrayexpress
Project description:The study objective was to propose molecular mechanisms of action of the histone deacetylase inhibitor vorinostat. In the PRAVO phase 1 study, patients that were scheduled to receive pelvic palliative radiation to 30 Gy in 3-Gy fractions for gastrointestinal carcinoma, were enrolled onto four sequential dose levels of vorinostat, starting at 100 mg daily with dose escalation in increments of 100 mg. Endpoints included treatment safety and tolerability, tumor response, and biological activity of vorinostat. For the purpose of identifying biomarkers of vorinostat action, peripheral blood mononuclear cells, representing normal tissue exposed to vorinostat, were used. The samples were collected, one at baseline and two on-treatment samples. The time points for sample collection were chosen based on our previous data from experimental colorectal carcinoma models exposed to vorinostat, demonstrating that the maximum tumor histone acetylation 2-3 hours after drug exposure was restored to baseline after 24 hours. In PRAVO study patients, tumor histone hyperacetylation was observed 3 hours after vorinostat administration. From the 17 patients enrolled onto the PRAVO study, a full set of three samples was obtained from 14 individuals: one baseline sample collected prior to commencement of vorinostat treatment (T0), and two on-treatment samples collected 2 and 24 hours after the patient had received the preceding daily dose of vorinostat (T2 and T24). Individual vorinostat dose levels were 100 mg (D100), 200 mg (D200), 300 mg (D300), or 400 mg (D400).
2013-05-08 | E-GEOD-46703 | biostudies-arrayexpress
Project description:To investigate the interaction landscape at the GILZ locus we performed 4C-seq in A549 (ATCC CCL-185) and U2OS cells stably expressing rat GR (Rogatsky et al. , Mol Cell Biol, 1997. 17(6): p. 3181-93.) upon hormone treatment (1.5 h, 1 M dexamethasone). Experiments were performed in two biological replicates using hg19 chrX:106,960,488-106,960,865 as a viewpoint.
2018-04-12 | E-MTAB-5350 | biostudies-arrayexpress
Project description:Normal donor blood was incubated with or without IFN-g stimulation to establish an IFN-g gene signature. Systemic lupus erythematosus subjects were treated with placebo or AMG 811, a therapeutic anti-IFN--g antibody, and changes in the IFN--g signature in whole blood of these subjects was measured. Blood from healthy volunteers (n=4) was collected into sodium heparin tubes, and then untreated or treated with 294 pM recombinant human IFN-γ for 0, 24, or 48 hours with incubation at 37oC, 5 % CO2. The blood was then added to PAXgene tubes and processed for RNA purification. Twenty six subjects with stable, mild to moderate SLE were administered placebo or a single dose of AMG 811 ranging from 2 mg to 180 mg SC or 60 mg IV. Whole blood PAXgene tube samples were collected from all cohorts at baseline, day-1 (pre-dose), and at days 15, 56, and end of study (EOS) after treatment Arrays were hybridized in a Loop design.
2016-02-24 | E-GEOD-78193 | biostudies-arrayexpress
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:The REVOLUTA and KANADI1 transcription factors act in opposite directions to control polarity in Arabidopsis. By analyzing mRNA profiles following activation of REVOLUTA or KANADI1 proteins we identified genes regulated by both transcription factors, focusing on those regulated in opposite directions. To coordinate transcriptional responses for microarray analysis, we constructed transgenic seedlings with the REV or KAN1 transcription factor fused to a glucocorticoid receptor (GR) domain. The GR domain tethers the transcription factor in the cytoplasm, and treatment with dexamethasone (DEX) allows movement into the nucleus. Transgenic seedlings and wild-type controls were grown simultaneously in liquid culture, treated with dexamethasone for 0min, 30min, 60min, or 120min, and total RNA was extracted and hybridized to Affymetrix arrays. Treatment: Dexamethasone Biological replicates
2013-12-31 | E-GEOD-30702 | biostudies-arrayexpress
Project description:In the present study, we investigated the importance of histone deacetylase 6 (HDAC6) for glucocorticoid receptor (GR) mediated effects on glucose metabolism, and its potential as a therapeutic target for the prevention of glucocorticoid (GC)-induced diabetes. Dexamethasone (dex)-induced hepatic glucose output and GR translocation were analysed in wildtype (wt) and HDAC6-deficient (HDAC6ko) mice. The effect of the specific HDAC6-inhibitor tubacin was analysed in-vitro. Wt and HDAC6ko mice were subjected to 3 weeks dex treatment before analysis of glucose and insulin tolerance. HDAC6ko mice showed impaired dex-induced hepatic GR translocation. Accordingly, dex induced expression of a large number of hepatic genes was significantly attenuated in mice lacking HDAC6 and by tubacin in-vitro. Glucose output of primary hepatocytes from HDAC6ko mice was diminished. A significant improvement of dex-induced whole-body glucose intolerance as well as insulin resistance in HDAC6ko mice compared to wt littermates was observed. The present study demonstrates that HDAC6 is an essential regulator of hepatic GC stimulated gluconeogenesis and impairment of whole body glucose metabolism through modification of GR nuclear translocation. Selective pharmacological inhibition of HDAC6 may provide a future therapeutic option against the pro-diabetogenic actions of GCs. In this dataset, we include the expression data obtained from isolated RNA of dissected mouse livers using wildtype and HDAC6 deficient animals which were treated over a timespan of 3 weeks with 1mg/kg dexamethasone and vehicle respectively. These data are used to show the hdac6-deficiency mediated attenuation of several dexamethasone induced genes. 12 samples in total were analyzed. 3 samples of different animals of each group (wt vehicle, wt dexamethasone, hdac6ko vehicle and hdac6ko dexamethasone)
2011-12-07 | E-GEOD-34229 | biostudies-arrayexpress