GR and Pol II interactions with regulatory elements in response to ultradian (pulsed) hormone stimulation [ChIP-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE61234 | GEO | 2015/02/12
SECONDARY ACCESSION(S): PRJNA260570
REPOSITORIES: GEO
Similar Datasets
Project description:We report changes in GR and Pol II binding profiles genome-wide upon treatment with corticosterone (Cort) for 20 minutes, treatment with Cort for 20 minutes followed by hormone withdrawal for 40 minutes, 60 minutes continuous stimulation with Cort, and 60 minutes continuous stimulation with Dexamethasone (Dex). We examine GR binding upon following treatments: 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant; Pol II binding upon following treatments: 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant, 60' Dex Constant; Pol II binding upon Mock treatments simulating 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant; CTCF binding profile of untreated cells.
2015-02-12 | E-GEOD-61234 | biostudies-arrayexpress
Project description:We report changes in DNaseI accessibility genome-wide upon treatment with corticosterone (Cort) for 20 minutes, treatment with Cort for 20 minutes followed by hormone withdrawal for 40 minutes, 60 minutes continuous stimulation with Cort, as well as Mock treatments for the aforementioned conditions.
2015-02-12 | GSE61235 | GEO
Project description:Three groups of Wistar rats with different manipulated levels of corticosterone were used to identify corticosteroid-responsive genes in hippocampus: 1. rats were adrenalectomised (ADX) 2. In addition to ADX these rats were implanted with a subcutaneous pellet containing 20 mg corticosterone and 80% cholesterol (ADX + low CORT) 3. In addition to ADX and implantation of a corticosterone pellet, these rats received a subcutaneous injection with corticosterone (1 mg/kg bodyweight) three hours prior to decapitation ((ADX + low CORT) + acute high CORT). All 3 groups of rats were decapitated three days after ADX and their hippocampus was isolated. Hippocampal RNA from 6 rats per group was pooled and used as input material for the SAGE libraries. Keywords: parallel sample
2003-10-30 | E-GEOD-787 | biostudies-arrayexpress
Project description:Three groups of Wistar rats with different manipulated levels of corticosterone were used to identify corticosteroid-responsive genes in hippocampus: 1. rats were adrenalectomised (ADX) 2. In addition to ADX these rats were implanted with a subcutaneous pellet containing 20 mg corticosterone and 80% cholesterol (ADX + low CORT) 3. In addition to ADX and implantation of a corticosterone pellet, these rats received a subcutaneous injection with corticosterone (1 mg/kg bodyweight) three hours prior to decapitation ((ADX + low CORT) + acute high CORT). All 3 groups of rats were decapitated three days after ADX and their hippocampus was isolated. Hippocampal RNA from 6 rats per group was pooled and used as input material for the SAGE libraries. Keywords: parallel sample
2003-10-31 | GSE787 | GEO
Project description:We have previously shown that corticosterone (CORT) can induce premature differentiation of somatotrophs in the chicken embryo. CORT induction of GH mRNA is indirect, in that protein synthesis inhibition blocks its inducing effect. In this study, we used a custom chicken microarray to analyze global gene expression in the embryonic pituitary gland and to identify potential direct targets of CORT that may regulate its induction of somatotroph differentiation. Our microarray analysis revealed 25 direct early targets of CORT. Keywords: Duration of corticosterone treatment on gene expression levels
2006-06-14 | GSE5067 | GEO
Project description:Aim: We investigated whether glucocorticoid effects on memory are associated with genomic interactions between the GR and pCREB in the hippocampus. Methods: Adult male rats received 3 minutes of object exploration training or no training either with a 3.0mg.kg post-training corticosterone injection or vehicle injection to study the molecular effects underlying enhanced memory formation. Hippocampi were dissected 45 minutes after injection and snap-frozen. Subsequently, Chromatin ImmunoPrecipitation was performed for GR and pCREB and the ChIP samples were sequenced.
2021-04-19 | GSE160806 | GEO
Project description:Although glucocorticoids (GCs) are known to exert numerous effects in the hippocampus, their chronic regulatory functions remain poorly understood. Moreover, evidence is inconsistent regarding the longstanding hypothesis that chronic GC exposure promotes brain aging/Alzheimer's disease. Here, we adrenalectomized male F344 rats at 15-months-of-age, maintained them for 3 months with implanted corticosterone (CORT) pellets producing low or intermediate (glucocorticoid-receptor (GR)-activating) blood levels of CORT, and performed microarray/pathway analyses in hippocampal CA1. We defined the chronic GC-dependent transcriptome as 393 genes that exhibited differential expression between Intermediate- and Low-CORT groups. Short-term CORT (4 days) did not recapitulate this transcriptome. Functional processes/pathways overrepresented by chronic CORT-upregulated genes included learning/plasticity, differentiation, glucose metabolism and cholesterol biosynthesis, whereas processes overrepresented by CORT-downregulated genes included inflammatory/immune/glial responses and extracellular structure. These profiles indicate that GCs chronically activate neuronal/metabolic processes while coordinately repressing a glial axis of reactivity/inflammation. We then compared the GC-transcriptome with a previously-defined hippocampal aging transcriptome, revealing a high proportion of common genes. Although CORT and aging moved expression of some common genes in the same-direction, the majority were shifted in opposite directions by CORT and aging (e.g., glial inflammatory genes downregulated by CORT are upregulated with aging). These results contradict the hypothesis that GCs simply promote brain aging, and also suggest that the opposite-direction shifts during aging reflect resistance to CORT regulation. Therefore, we propose a new model in which aging-related GC resistance develops in some target pathways while GC overstimulation develops in others, together generating much of the brain aging phenotype. Forty male Fischer 344 rats aged 14-15 months (late mid-age) were either sham operated (n=10) or adrenalectomized (n=30) at Harlan, Inc. (Indianapolis) and shipped to University of Kentucky 7-10 d after surgery. Animals were allowed to acclimate for 2 weeks after receipt prior to pellet-implant and were provided with food and water ad lib. Adrenalectomized (ADX) animals were maintained on drinking water containing isotonic saline with 1% sucrose, and also given supplemental feed mash (standard chow mixed with water and warmed) and apple chunks, as well as subcutaneous injections of 1.25 mg corticosterone sulfate (Solu-DeltaCort, Pfizer). During pellet-implant surgery, subjects were anesthetized with isoflurane, placed on a warming pad, and a 3 cm2 area on the animal's flank was shaved and sterilized. A 1-cm incision was made through the skin to form a subcutaneous pocket. Each sham animal received an inert pellet. ADX animals were divided into two groups, low-dose animals (n = 20) received one 25 mg CORT pellet and intermediate-dose animals (n = 10) received one 200 mg CORT pellet (slow release pellets, Innovative Research of America, Sarasota, FL). Incisions were closed with wound clips (removed after 7-10 days). Following implant surgery, subjects were housed singly for 3 months prior to euthanasia at age 18 months. Low-dose animals continued to receive saline/ sucrose drinking water, but other supplementation (food mash, Solu-Delta CORT, apple chunks) was discontinued. One ADX animal was removed from the study for declining health. During the twelfth week, just prior to study termination, half of the ADX low-dose CORT subjects were given a short-term, high-dose regimen consisting of 4 daily IP injections of 5mg/d CORT (considered a relatively high dose- Makino et al., 1995). All animals were killed between 8 and 10 AM on the last two days of the study. After deep CO2 anesthesia and decapitation, trunk blood was collected for CORT radioimmunoassay and hippocampal CA1 brain tissue was dissected as described previously (Blalock et al., 2003) for microarray analysis (see below). Final treatment groups consisted of: 1) Sham (intact) control, 2) Low-CORT (ADX), 3) Intermediate-CORT (ADX), and 4) Low-CORT (ADX) + short-term high-dose injected (n=9-10/group).
2013-07-22 | E-GEOD-37618 | biostudies-arrayexpress
Project description:Male Sprague-Dawley rats 8 weeks old, were adrenalectomized, treated with 300ug/kg corticosterone or vehicle 3 days after surgery then sacrificed 1 hour later. Hippocampi were removed and RNA extracted and processed for sequencing at the Massachusetts General Hospital Nex-Generation Sequening Core. Includes 6 cort treated and 6 control biological replicates
2016-08-11 | E-GEOD-84249 | biostudies-arrayexpress
Project description:The binding of the glucocorticoid receptor (GR to GR regulatory elements (GREs) over constant treatment with 600nM corticosterone (Cort) changes over time in a locus-specific manner. We show this by comparing GR binding at 0h, 1h, and 12h after Cort treatment. This finding is further corroborated by the reduced dwell times of GR over time measured by single molecule tracking (SMT) as well as by the reduced RNA bust duration and frequency observed at the GR-mediated mouse mammary tumor promoter (MMTV) transcription sites (TSs).
2019-06-13 | GSE132502 | GEO
Project description:Although glucocorticoids (GCs) are known to exert numerous effects in the hippocampus, their chronic regulatory functions remain poorly understood. Moreover, evidence is inconsistent regarding the longstanding hypothesis that chronic GC exposure promotes brain aging/Alzheimer's disease. Here, we adrenalectomized male F344 rats at 15-months-of-age, maintained them for 3 months with implanted corticosterone (CORT) pellets producing low or intermediate (glucocorticoid-receptor (GR)-activating) blood levels of CORT, and performed microarray/pathway analyses in hippocampal CA1. We defined the chronic GC-dependent transcriptome as 393 genes that exhibited differential expression between Intermediate- and Low-CORT groups. Short-term CORT (4 days) did not recapitulate this transcriptome. Functional processes/pathways overrepresented by chronic CORT-upregulated genes included learning/plasticity, differentiation, glucose metabolism and cholesterol biosynthesis, whereas processes overrepresented by CORT-downregulated genes included inflammatory/immune/glial responses and extracellular structure. These profiles indicate that GCs chronically activate neuronal/metabolic processes while coordinately repressing a glial axis of reactivity/inflammation. We then compared the GC-transcriptome with a previously-defined hippocampal aging transcriptome, revealing a high proportion of common genes. Although CORT and aging moved expression of some common genes in the same-direction, the majority were shifted in opposite directions by CORT and aging (e.g., glial inflammatory genes downregulated by CORT are upregulated with aging). These results contradict the hypothesis that GCs simply promote brain aging, and also suggest that the opposite-direction shifts during aging reflect resistance to CORT regulation. Therefore, we propose a new model in which aging-related GC resistance develops in some target pathways while GC overstimulation develops in others, together generating much of the brain aging phenotype.
2013-07-22 | GSE37618 | GEO