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: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: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
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:Maternal exposure to estrogens can induce long-term adverse effects in the offspring. This may be mediated through alterations in the endometrium affecting embryo-maternal communication as early as the preimplantational phase. Thus, we analyzed the effects of gestational estradiol-17β (E2) exposure on the endometrium. Two distinct low doses and a high dose (0.05, 10 and 1000 µg E2/kg body weight daily, respectively) were orally applied to sows from insemination until sampling at day 10 of pregnancy and compared to carrier-treated controls. RNA-sequencing revealed a dose-dependent increase of 14, 17 and 27 differentially expressed genes (DEG), respectively. Overall, the maternal E2 treatment perturbed gene expression of the endometrium, potentially altering the uterine histotroph.
2018-10-16 | E-MTAB-6242 | biostudies-arrayexpress
Project description:In the fetal sheep during late gestation sulfoconjugated estrogens in plasma reach a concentration 40-100 times greater than unconjugated estrogens. The objective of the present study was to determine the genomics of estradiol-3-sulfate (E2S) action in the fetal brain. The hypothesis was that E2S stimulates genes involved in the neuroendocrine pathways in the hypothalamus that direct or facilitate fetal development at the end of gestation. Four sets of chronically-catheterized ovine twin fetuses were studied (gestational age: 120-127 days gestation) with one infused with E2S intracerebroventricularly (1 mg/day) and the other remained untreated (control). After euthanasia, mRNA samples were extracted from the 8 hypothalami, corresponding to the four treatment and four control fetuses. Microarray analysis was performed following the Agilent protocol for 1-color 8x15 microarrays, designed for Ovis aries.
2011-08-03 | GSE31184 | GEO
Project description:Estradiol Induced Transcriptional Profile of EAAE DNA Binding Deficient ERa Uterus
| PRJNA243280 | ENA
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:To uncover genes regulated by mTORC1 and estradiol in uterine Tsc2-null LAM like cells, we performed RNAseq on uteri from 12-week old wild-type (WT) and uterine-specific Tsc2-null (KO) mice that were either untreated (intact), oopherectomized (ovx) or oopherectomized + treated with 17β-estradiol pellets (E2) for 8 weeks. We identified genes that were both estradiol- and TSC2-mediated. Uterine mRNA profiles of 12 week old wild type (WT) and uterine-specific Tsc2-null (KO) mice in the presence or absence of estradiol were generated using Illumina HiSeq2500
2016-02-26 | E-GEOD-78701 | biostudies-arrayexpress
Project description:Treatment with the breast cancer drug tamoxifen confers a risk of developing uterine tumors or other endometrial pathologies. Tamoxifen is a selective estrogen receptor modulator, which demonstrates tissue-specific activity although the mechanisms remain poorly understood. Both estradiol and tamoxifen act as estrogen agonists on the human uterus, and therefore have the potential to promote carcinogenicity. Estradiol and tamoxifen elicit cellular responses via the estrogen receptors (ER), which are involved in multiple signalling pathways. The effects at the molecular level are further influenced by the differential recruitment of co-factors and the presence of specific promoter motifs in target genes. In this study, ER positive (+) Ishikawa cells are used as a model to investigate the overall effect of treatment with either 17b-estradiol or 4-hydroxytamoxifen on the gene expression profiles. Keywords: Comparison of estradiol and tamoxifen on Ishikawa human uterine cells after 24h or 48h
2006-02-01 | GSE3762 | GEO