E-MTAB-6263
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6263 | ExpressionAtlas | 2019-09-09
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-6263-analysis-methods.tsv | Tabular | |||
| E-MTAB-6263-analytics.tsv | Tabular | |||
| E-MTAB-6263-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-6263-configuration.xml | Xml | |||
| E-MTAB-6263-g1_g2-mvaPlot.png | Other |
Items per page: 5 1 - 5 of 38 |
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Project description:Preimplantational estrogen exposure to pregnant gilts has been associated with implantation failure, embryonic losses and changes in endometrial mRNA expression. Small non-coding RNAs (ncRNA), especially miRNAs, play a key role in regulation of gene expression. Effects of estrogens on endometrial microRNAs (miRNA), however, have not been investigated in this context so far. Thus, we studied the influence of estradiol-17β (E2) on the endometrial expression profile of miRNAs in the pig at gestational day 10. E2 administered early during pregnancy resulted in significantly higher endometrial estrogen concentrations even at a low dose, but did not disrupt the expression profile of endometrial miRNAs.
2018-03-21 | GSE89343 | GEO
Project description:RNA-seq of estrogen (E2) induced changes of mRNA expression in male and female blastocysts.
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Project description:E2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17β-estradiol (E2) or select estrogen receptor modulators (SERMs), then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects where sex-dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor- 2 (ESR2) as neither genomic ESR1 nor non- genomic GPR30 were expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion, but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans.
2015-12-31 | GSE75208 | GEO
Project description:Human embryonic stem cell-derived thyroid follicles were exposed for 3 days to a mixture of the sex hormones beta-estradiol (E2), 5-alpha-dihydrotestosterone (DHT) and progesterone (PG) that resemble the serum levels of human male and female (post-ovulation) of reproductive age. Afterwards, they were exposed for 1 day to the mixtures of sex hormones + 10 uM benzo[a]pyrene (BaP) or 10 uM PCB153. At the end of the treatment period, organoids were dissociated into single cell suspension and single cell RNA-Sequencing (scRNA-Seq) performed.
2024-08-29 | E-MTAB-13502 | biostudies-arrayexpress
Project description:E2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17β-estradiol (E2) or select estrogen receptor modulators (SERMs), then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects where sex-dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor- 2 (ESR2) as neither genomic ESR1 nor non- genomic GPR30 were expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion, but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans. Primary human nasal epithelial cells from females were exposed to E2 for 24h prior to infection, then infected with an H3N2 strain of influenza a virus for 2 hours. At 24 and 48h post infection, hNECs were collected in Trizol for RNA extraction and hybridization on Affymetrix Human Gene ST 2.0 microarrays.
2015-12-31 | E-GEOD-75208 | biostudies-arrayexpress
Project description:Environmental estrogens may affect epigenetic programming as early as the period of preimplantation development. Therefore, we analyzed the effects of continuous gestational estradiol-17β (E2) exposure on male and female embryos. A low dose, close to the no-observed effect level (NOEL - 10 µg E2/kg body weight(bw)/d), a high dose (1000 µg E2/kg bw/d) and carrier only, as control group, was fed to sows from insemination until sampling at day 10 of pregnancy, respectively. 36 samples (n = 5-7 per treatment group and sex) were analyzed by high throughput sequencing.In the high dose group, RNA-sequencing of single embryos revealed 982 differentially expressed genes (DEG) in the female but none in the male blastocysts. Moreover, 62 and 3 DEG were found in female and male embryos of the NOEL dose group, respectively. Thus, maternal E2 treatment during early pregnancy affected gene expression of the embryos at day 10, potentially constituting the basis for long-term adverse effects.
2018-10-16 | E-MTAB-6263 | biostudies-arrayexpress
Project description:Adult male goldfish, exposed to estrogen (E2) implant, 1 day exposure See the following for further details; Marlatt VL, Martyniuk, CJ, Zhang, D, Xiong, H, Xia, X, Trudeau, VL, Moon, T. Tissue-specific auto-regulation of estrogen receptor subtypes and transcript profiling of estrogen-responsive genes in the neuroendocrine brain of male goldfish (Carassius auratus) exposed to 17beta-estradiol. J. Mol. Endocrinol. (accepted). Keywords: Estrogen effect on male goldfish hypothalamus, microarray
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Project description:Developmental exposure of mouse fetuses to estrogens results in dose-dependent permanent effects on prostate morphology and function. Fetal prostatic mesenchyme cells express estrogen receptor alpha (ERα) and androgen receptors and convert stimuli from estrogens and androgens into signaling to regulate epithelial cell proliferation and differentiation. To obtain mechanistic insight into the role of different doses of estradiol (E2) in regulating mesenchymal cells, we examined E2-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells. Urogenital sinus mesenchyme cells were obtained from male mouse fetuses at gestation day 17 and exposed to 10 pM, 100 pM or 100 nM E2 in the presence of a physiological concentration of dihydrotestosterone (0.69 nM) for four days. Gene ontology studies suggested that low doses of E2 (10 pM and 100 pM) induce genes involved in cell adhesion, morphological tissue development, and sterol biosynthesis but suppress genes involved in growth factor signaling and cell adhesion. Genes showing inverted-U-shape dose responses (enhanced by E2 at 10 pM E2 but suppressed at 100 pM) were identified, and their enrichment in the glycolytic pathway was demonstrated. At the highest dose (100 nM), E2 induced genes enriched not only for cell adhesion but also steroid hormone signaling and metabolism, cytokines and their receptors, cell-to-cell communication, Wnt signaling, and TGF-β signaling. These results suggest that prostate mesenchymal cells may regulate epithelial cells through direct cell contacts when estrogen level is low whereas soluble growth factors might play significant roles when estrogen level is high.
2012-03-21 | GSE36630 | GEO
Project description:Developmental exposure of mouse fetuses to estrogens results in dose-dependent permanent effects on prostate morphology and function. Fetal prostatic mesenchyme cells express estrogen receptor alpha (ERα) and androgen receptors and convert stimuli from estrogens and androgens into signaling to regulate epithelial cell proliferation and differentiation. To obtain mechanistic insight into the role of different doses of estradiol (E2) in regulating mesenchymal cells, we examined E2-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells. Urogenital sinus mesenchyme cells were obtained from male mouse fetuses at gestation day 17 and exposed to 10 pM, 100 pM or 100 nM E2 in the presence of a physiological concentration of dihydrotestosterone (0.69 nM) for four days. Gene ontology studies suggested that low doses of E2 (10 pM and 100 pM) induce genes involved in cell adhesion, morphological tissue development, and sterol biosynthesis but suppress genes involved in growth factor signaling and cell adhesion. Genes showing inverted-U-shape dose responses (enhanced by E2 at 10 pM E2 but suppressed at 100 pM) were identified, and their enrichment in the glycolytic pathway was demonstrated. At the highest dose (100 nM), E2 induced genes enriched not only for cell adhesion but also steroid hormone signaling and metabolism, cytokines and their receptors, cell-to-cell communication, Wnt signaling, and TGF-β signaling. These results suggest that prostate mesenchymal cells may regulate epithelial cells through direct cell contacts when estrogen level is low whereas soluble growth factors might play significant roles when estrogen level is high. Primary culture urogenital sinus mesenchymal cells were isolated from prostate glands of gestation day 17 CD1 male mouse fetuses. Cells were then exposed to 10 pM or 100 pM 17beta-estradiol or vehicle (0.05% ethanol) for four days in the presence of 690 pM 5alpha-dihydrotestosterone. Total cellular RNA was then isolated for determination of transcriptomal profiles by Affymetrix mouse gene 1.0 ST array.
2012-03-21 | E-GEOD-36630 | biostudies-arrayexpress
Project description:Simple Markov model.
There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal.
The yearly transition probabilities are:
Healthy to Dead: 0.01; Healthy to Sick: 0.2 for Male and 0.1 for Female; Sick to Healthy: 0.1; Sick to Dead: 0.3.
The transition probability now depends on the cohort (Male or Female) and can be expressed as a function of a Boolean covariate Male.
Initial conditions: Healthy = (50 Male, 50 Female), Sick = (0,0) and Dead = (0,0).
Output: Number of men and women in each disease state for years 1-10.
2019-01-30 | MODEL1803120004 | BioModels