Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA262681 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional responses in ovariectomized mouse uterine tissue to estradiol (E2) and diethylstilbestrol (DES), known long-acting estrogens, and propyl pyrazole triol (PPT), an ER-alpha selective estrogen, were profiled. Profiles were used together with those from other estrogens to derive a biomarker panel.
2015-10-01 | GSE61921 | GEO
Project description:We used gene expression profiling to investigate whether the molecular effects induced by estrogens of different provenance are intrinsically similar. In this article we show that the physiologic estrogen 17-beta-estradiol, the phytoestrogen genistein, and the synthetic estrogen diethylstilbestrol alter the expression of the same 179 genes in the intact immature mouse uterus under conditions where each chemical has produced an equivalent gravimetric and histologic uterotrophic effect, using the standard 3-day assay protocol. Data are also presented indicating the limitations associated with comparison of gene expression profiles for different chemicals at times before the uterotrophic effects are fully realized. We conclude that the case has yet to be made for regarding synthetic estrogens as presenting a unique human hazard compared with phytoestrogens and physiologic estrogens. Key words: diethylstilbestrol, estrogen, gene expression, genistein, microarray, phytoestrogen, toxicogenomics, uterus.
2022-11-20 | E-AFMX-13 | biostudies-arrayexpress
Project description:This experiment investigates the functional roles of estrogen receptor alpha and beta in peripheral blood leukocytes by using selective estrogen receptor agonists. The agonists that are used are estradiol (E2), the selective ER-alpha agonist PPT (4,4',4''-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol) and the selective ER-beta agonist DPN (2,3-bis(4-hydroxyphenyl)-propionitrile).
2007-05-30 | E-TABM-269 | biostudies-arrayexpress
Project description:To investigate the molecular mechanisms by which estrogen receptor α (ERα) inhibits type I IFN-induced signaling. We identified genes induced by ERα signaling using data obtained from RNA-seq of MCF7 cells treated or untreated with selective ERα agonist propyl pyrazole triol (PPT).
2022-05-18 | GSE203058 | GEO
Project description:A toxicity pathway approach was taken to develop an in vitro assay using human uterine epithelial adenocarcinoma (Ishikawa) cells (ECACC cat#99040201) as a replacement for measuring an in vivo uterotrophic response to estrogens. As part of validating the use of this cell line, gene arrays were performed to confirm functional transcriptional responses to ethinyl estradiol (EE)
2017-07-01 | GSE84711 | GEO
Project description:Previously, we described a mouse model where the well-known reproductive carcinogen, diethylstilbestrol (DES), caused uterine adenocarcinoma following neonatal treatment. Tumor incidence was dose-dependent reaching >90% by 18 mo. following 1000 µg/kg/day of DES. These tumors followed the initiation/promotion model of hormonal carcinogenesis with developmental exposure as the initiator, and exposure to ovarian hormones at puberty as the promoter. To identify molecular pathways involved in DES-initiation events, uterine gene expression profiles were examined in prepubertal mice exposed to DES (1, 10 or 1000 µg/kg/day) on days 1-5 and compared to age-matched controls. Of more than 20,000 transcripts, approximately 3% were differentially expressed in at least one DES treatment group compared to controls; several transcripts demonstrated dose-responsiveness. Assessment of gene ontology annotation revealed alterations in genes associated with cell growth, differentiation, and adhesion. When expression profiles were compared to published studies of uteri from 5 day old DES-treated mice, or adult mice treated with 17β estradiol, similarities were seen suggesting persistent differential expression of estrogen responsive genes following developmental DES exposure. Moreover, several significantly altered genes have been identified in human uterine adenocarcinomas. Four altered genes [Lactotransferrin (Ltf), Transforming growth factor beta inducible (Tgfβ1), Cyclin D1 (Ccnd1), and Secreted frizzled-related protein 4 (Sfrp4)], selected for real time RT-PCR analysis, correlated well with the directionality of the microarray data. These data suggest altered gene expression profiles observed two weeks after treatment ceased, were imprinted at the time of developmental exposure and maybe related to the initiation events resulting in carcinogenesis. Keywords: dose reponse
2007-06-14 | GSE5825 | GEO
Project description:The goal of this study was to identify a set of hepatic genes regulated by ligand-dependent activation of the estrogen receptor in juvenile rainbow trout (Oncorhynchus mykiss) that can serve as a biomarker of estrogen exposure. A custom rainbow trout oligo DNA microarray, which contains probes targeting approximately 1450 genes relevant to carcinogenesis, toxicology, endocrinology and stress physiology was utilized to identify transcriptional “fingerprints” of in vivo dietary exposure to 17β-estradiol (E2), tamoxifen (TAM), estradiol + tamoxifen (E2+TAM), diethylstilbestrol (DES), dehydroepiandrosterone (DHEA), dihydrotestosterone (DHT) and cortisol (CORT). Estrogen exposure altered the expression of up to 49 genes involved in reproduction, immune response, cell growth, transcriptional regulation, protein synthesis and modification, drug metabolism, redox regulation and signal transduction. E2, DES and DHEA regulated 18 genes in common, mostly those associated with vitellogenesis, cell proliferation and signal transduction. Interestingly, DHEA uniquely regulated several complement component genes of importance to immune response. While the effect of TAM on E2-induced changes in gene expression was mostly antagonistic, TAM alone increased expression of VTG1 and other genes associated with egg development and immune response. Few genes responded to CORT treatment, and DHT significantly altered expression of only one gene targeted by the OSUrbt array. Hierarchical cluster and principal components analyses revealed distinct patterns of gene expression corresponding to estrogens and non-estrogens, though unique patterns could also be detected for individual chemicals. A set of estrogen-responsive genes has been identified that can serve as a biomarker of environmental exposure to xenoestrogens. Keywords: estrogen transcriptional profile, chemical transcriptional fingerprint
2007-07-13 | GSE8226 | GEO
Project description:Previously, we described a mouse model where the well-known reproductive carcinogen, diethylstilbestrol (DES), caused uterine adenocarcinoma following neonatal treatment. Tumor incidence was dose-dependent reaching >90% by 18 mo. following 1000 µg/kg/day of DES. These tumors followed the initiation/promotion model of hormonal carcinogenesis with developmental exposure as the initiator, and exposure to ovarian hormones at puberty as the promoter. To identify molecular pathways involved in DES-initiation events, uterine gene expression profiles were examined in prepubertal mice exposed to DES (1, 10 or 1000 µg/kg/day) on days 1-5 and compared to age-matched controls. Of more than 20,000 transcripts, approximately 3% were differentially expressed in at least one DES treatment group compared to controls; several transcripts demonstrated dose-responsiveness. Assessment of gene ontology annotation revealed alterations in genes associated with cell growth, differentiation, and adhesion. When expression profiles were compared to published studies of uteri from 5 day old DES-treated mice, or adult mice treated with 17β estradiol, similarities were seen suggesting persistent differential expression of estrogen responsive genes following developmental DES exposure. Moreover, several significantly altered genes have been identified in human uterine adenocarcinomas. Four altered genes [Lactotransferrin (Ltf), Transforming growth factor beta inducible (Tgfβ1), Cyclin D1 (Ccnd1), and Secreted frizzled-related protein 4 (Sfrp4)], selected for real time RT-PCR analysis, correlated well with the directionality of the microarray data. These data suggest altered gene expression profiles observed two weeks after treatment ceased, were imprinted at the time of developmental exposure and maybe related to the initiation events resulting in carcinogenesis. Experiment Overall Design: There were 3 DES doses (1, 10 and 1000 ug/kg/day) administered to neonates on days 1-5. RNA was pooled for 10 mice, with each dose having its own matching control (corn oil). Dye-flipped hybridizations were performed for each paired comparison.
2008-11-06 | E-GEOD-5825 | biostudies-arrayexpress
Project description:Neonatal diethylstilbestrol exposure alters the metabolic profile of uterine epithelial cells.
| PRJNA166857 | ENA
Project description:Estrogens stimulate hypertrophy and hyperplasia in the uterus and exert their activity through estrogen receptor α (ERα). A uterine epithelial ERα conditional knockout mouse model (Wnt7aCre+;Esr1f/f or cKO) demonstrated that ERα in the epithelial cells was dispensable for an early uterine proliferative response to 17β-estradiol (E2), but required for subsequent uterine biological responses. We compared the gene expression profile in the uterus after E2 treatment in the cKO samples with WT samples. We found that approximately 25% of the genes differentially expressed at 2 h were epithelial ERα independent, as they were preserved in the cKO, indicating they are mediated from the stroma and sufficient to promote initial proliferative responses. However, more than 90% of the differentially expressed transcripts at 24 h were absent in the cKO, indicating the majority of later transcriptional regulation required epithelial ERα and suggesting the loss of regulation of these later transcripts results in the blunted growth response 3 days after treatment. These transcription profiles correlate with our previous biological responses, in which the initial proliferative response is independent of epithelial ERα but dependent on stromal ERα, yet epithelial ERα is essential for subsequent tissue responsiveness. These analyses are now allowing for in vivo determination of the cell specific actions of ERα in the female reproductive tract.
2014-12-01 | GSE53812 | GEO