Comparison of cortisol metrics and total RNA profiles from Healthy Individuals
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE134637 | GEO | 2020/07/31
REPOSITORIES: GEO
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Project description:Comparison of cortisol metrics and total RNA profiles from Healthy Individuals
| PRJNA555899 | ENA
Project description:The present work was designed to assess the effects of high plasma cortisol levels induced by slow-release cortisol implants in the mRNA transcription of the GR in the different organs of the Sparus aurata, including liver. For that purpose fish were intraperitoneally injected with the implants containing two different concentrations of cortisol (50 or 200 µg/g body weight) and blood and organs were sampled after 7 and 14 days of implantation. Only fish with 200 µg/g implants exhibited a significant rise in the plasma cortisol.
2011-07-20 | GSE30782 | GEO
Project description:The present work was designed to assess the effects of high plasma cortisol levels induced by slow-release cortisol implants in the mRNA transcription of the GR in the different organs of the Sparus aurata, including liver. For that purpose fish were intraperitoneally injected with the implants containing two different concentrations of cortisol (50 or 200 µg/g body weight) and blood and organs were sampled after 7 and 14 days of implantation. Only fish with 200 µg/g implants exhibited a significant rise in the plasma cortisol. For microarray analysis we used livers of gilthead sea bream (N=36 fish). Fish were injected with 200 µg/g body weight of cortisol and sampled after 7 and 14 days (n=6 for each condition). RNA samples were grouped into pools of 2 animals for each time point. The analysis were carried out considering the transcripts differentially expressed in the group of fish implanted during 7 days with cortisol comparing to control group. Additionally, the transcripts differentially expressed at day 14 were compared with day 7.
2011-07-19 | E-GEOD-30782 | biostudies-arrayexpress
Project description:Glucocorticoids act through the glucocorticoid receptor (GR), a ligand activated transcription factor, to modulate gene expression profiles in target cells and tissues. The principal physiological glucocorticoid in humans, cortisol, is released in a pulsatile fashion from the adrenal gland, which results in oscillations in blood concentrations, with a period of 1 - 2 hours. The biological consequence of fluctuating cortisol concentrations has not been explored. To identify the role of cortisol concentration oscillations for target cell response a flow-through cell culture system was developed. Transcription profiling was performed in the absence and presence of cortisol. Cells were exposed to constant cortisol levels of 100ng/ml or 200 ng/ml or oscillating cortisol concentrations.
2010-07-10 | E-MEXP-2447 | biostudies-arrayexpress
Project description:Transcriptional profiling of log and stationary phases of S. Typhimurium, comparing untreated controls with cortisol-treated samples. Each array used labelled cDNA against a common genomic DNA reference. Triplicate arrays were carried out for each of the 4 conditions: untreated log phase, untreated stationary phase, cortisol treated log phase and cortisol treated stationary phase.
2011-07-25 | E-GEOD-30923 | biostudies-arrayexpress
Project description:Chronic early life stress increases adult susceptibility to numerous health problems linked to chronic inflammation. One way that this may occur is via glucocorticoid-induced developmental programming. To gain insight into such programming, we treated zebrafish embryos with cortisol and examined the effects on adults. In adulthood, the treated fish maintained elevated basal cortisol levels in the absence of exogenous cortisol, and constitutively mis-expressed genes involved in defense response and its regulation. Adults derived from cortisol-treated embryos displayed defective tailfin regeneration, heightened basal expression of pro-inflammatory genes, and failure to appropriately regulate those genes following injury or immunological challenge. These results support the hypothesis that chronically elevated glucocorticoid signaling early in life directs development of a pro-inflammatory adult phenotype, at the expense of immunoregulation and somatic regenerative capacity.
2016-06-01 | GSE80260 | GEO
Project description:Purpose: Offspring from females that experience stressful conditions during reproduction often exhibit altered phenotypes and many of these effects are thought to arise due to increased exposure to maternal glucocorticoids. Here we used RNAseq to test whether the embryonic transcriptional response to increased levels of cortisol was similar to the transcriptional response to maternal stress in sticklebacks Methods: Eggs were treated by immersing eggs for 30 mins in water that contained 0, 5, or 10 ug/L, which represented baseline, predator induced, and super physiological levels of maternally derived cortisol. To isolated enough RNA for RNAseq, 10 embyros from each clutch/treatment were pooled prior to RNA extraction for a total of 18 pools (6 clutches x 3 treatments). Results: Analysis of genome-wide transcriptional profiles suggests that 17251 (genes which survived a cut-off of having cpm more than 1 in at least two samples; and had a significant likelihood ratio calculated in edgeR) genes out of the possible 22,456 genes in the stickleback genome were expressed in 72-hour embryos. However, we did not detect any differences in gene expression between embryos that were treated with cortisol compared to the control group. mRNA profiles of egg clutches treated with 0, 5, or 10 ug/L are compared, which represented baseline, predator induced, and super physiological levels of maternally derived cortisol.
2015-08-03 | E-GEOD-71649 | biostudies-arrayexpress
Project description:Transcriptional profiling of log and stationary phases of S. Typhimurium, comparing untreated controls with cortisol-treated samples.
2011-07-26 | GSE30923 | GEO
Project description:Background: Autonomous cortisol secretion (ACS), results from cortisol-producing adenomas (CPA), causes endogenous steroid-induced osteoporosis (SIOP). However, how other adrenal steroid metabolites affect bone status is unclear. Methods: ACS was diagnosed at serum cortisol after 1-mg dexamethasone suppression test (DST-cortisol) ≥ 1.8 g/dL. Using liquid chromatography-tandem mass spectrometry, we measured 21 plasma steroid metabolites in 73 patients with ACS and 85 with non-functioning adrenal tumors (NFAT). We also examined expression of steroidogenic enzymes and relevant steroid metabolites in some of CPA tissues. Results: In discriminant and principal component analysis, steroid profiles distinguished between the ACS and NFAT groups in premenopausal women. Premenopausal women with ACS exhibited higher levels of a mineralocorticoid metabolite; 11-deoxycorticosterone (11-DOC), with lower androgen metabolites; dehydroepiandrosterone-sulfate and androsterone-glucuronide. In premenopausal women with ACS, DST-cortisol was negatively correlated with trabecular bone score (TBS). Additionally, 11-DOC was negatively correlated with lumbar spine-bone mineral density (r = -0.603), while androsterone-glucuronide was positively correlated with TBS (r = 0.681), which was supported by Bayesian kernel machine regression analysis. There were no such correlations in postmenopausal women and men. The CPA tissues showed increased levels of 11-DOC, with increased expression of CYP21A2, which is essential for 11-DOC synthesis. The adrenal non-tumor tissues were atrophied with reduced expression of CYB5A, which is required for androgen synthesis. Conclusion: This study provides the first evidence that unbalanced production of adrenal steroid metabolites, which are derived from both adrenal tumors and non-tumor tissues, play a role in the pathogenesis of endogenous SIOP in premenopausal women with ACS.
2023-06-01 | E-MTAB-12895 | biostudies-arrayexpress
Project description:Cortisol administration during late gestation in ewes, modeling maternal stress, resulted in transcriptomic changes suggesting altered maturation and metabolic changes to the offspring heart. This study investigates the effects of cortisol on epicardial adipose tissue (EAT), a visceral fat pad associated with adverse cardiovascular conditions in adults. Pregnant ewes were treated with either 1 or 0.5 mg/kg/day cortisol from 115 days gestation to term and EAT collected from term fetuses (control: n=8, maternal cortisol 1 mg/kg/day: n=6) or two-week-old lambs (control: n=7, maternal cortisol 0.5mg/kg/day: n=9). Transcriptomic modeling was used to identify pathways altered by maternal cortisol over-exposure. Transcriptomic modeling confirmed the brown fat phenotype of EAT at term and a transition towards white fat at two weeks of age in EAT of control fetuses/lambs, and highlighted a role of immune responses, including complement-coagulation, and serotonin in this transition. Maternal cortisol (1mg/kg/day) increased the lipid peroxidation product 4-hydroxynonenal in EAT of term fetuses, but did not affect the number of activated macrophages or size of the lipid droplets in the depot; transcriptomics suggested an earlier metabolic maturation of EAT via, in part, increased immune responses. Conversely the transcriptomics in EAT of two-week-old lambs of ewes treated with a lower dose of cortisol (0.5mg/kg/day) suggested decreased metabolism of several substrates through both mitochondrial and cytosolic actions, and delayed maturation of EAT associated with a longer period of adipogenesis and angiogenesis.
2019-07-10 | GSE119254 | GEO