Time course experiment of 17β-estradiol (E2) treatment in the zebrafish
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE45562 | GEO | 2013/06/28
SECONDARY ACCESSION(S): PRJNA194579
REPOSITORIES: GEO
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Project description:Transcriptional profiling of zebrafish (Danio rerio) livers comparing control untreated fish with fish treated with estrogen [17β-estradiol (E2)] for different time points (4, 12, 24, 48 hours). For the assay experimental design, RNA from one of three different E2-treated fish (representing three biological replicates) of each time point was hybridized with RNA that was pooled from liver samples of 15 untreated fish (control pool) on one chip.
2013-06-28 | E-GEOD-45562 | biostudies-arrayexpress
Project description:Corpus luteum (CL) is a transient endocrine tissue formed from the remnants of the ovarian follicle after ovulation. In response to gonadotropin surge, the ovulating follicle undergoes dramatic changes in expression of genes and differentiation of follicular cells into luteal cells. In several species, of the several genes that are down- regulated post ovulation, Cyp19A1 that codes for aromatase, essential for biosynthesis of estradiol- 17β (E2), also get down- regulated but appears to get up- regulated at later time points in the estrous cycle to have critical role in E2 secretion. In primates and rodents, higher expression and higher E2 levels has been observed in CL. Surprisingly, in the recently carried out gene expression profiling of PGF2α- induced luteolysis studies in the bovine species [GSE27961], it was observed that expression of one of the earliest genes that was down- regulated was Cyp19A1 in the CL. However, the specific role of E2 in the regulation of CL function remains poorly defined. Thus, in the present study, efforts were made to examine the temporal changes in the global gene expression profile in the CL of pregnant rats after treatment with aromatase inhibitor (AI), Anastrozole, and E2 supplementation. The results obtained will further expand our knowledge on E2 target/responsive genes and the basic mechanism(s) that regulates the CL function. Key words: CL, E2, AI, Gene expression
2012-10-23 | GSE41735 | GEO
Project description:Transcriptional profiling of mussel (Mytilus galloprovincialis) digestive gland tissue comparing control tissue with tissue obtained from animals exposed to sublethal amounts of Chlorpyrifos, animals injected into the posterior adductor muscle with 25 pico-moles 17β-estradiol (E2) and animals pre-exposed for three days to the pesticide and further injected with E2. Background: Many pesticides have been shown to act as endocrine disrupters. Although the potencies of currently used pesticides as hormone agonists/antagonists in vitro are low compared with those of natural ligands, their ability to act via multiple mechanisms might enhance the biological effect. The organophosphate Chlorpyrifos (CHP) has been shown to be weakly estrogenic and cause adverse neurodevelopmental effects in mammals. However, no information is available on the possible endocrine effects of CHP in aquatic organisms. In the digestive gland of the bivalve Mytilus galloprovincialis, a target tissue for the action of both estrogens and pesticides, the possible effects of CHP on the responses to the natural estrogen 17β-estradiol (E2) were investigated. Methodology/Principal findings: Mussels were exposed to CHP (4.5 mg/l, 72 hrs) and subsequently injected with E2 (6.75 ng/g dw). Responses were evaluated in CHP, E2 and CHP/E2 treatment groups at 24 h p.i. by a biomarker/transcriptomic approach. CHP and E2 induced additive, synergistic, and antagonistic effects on lysosomal biomarkers (lysosomal membrane stability, lysosome/cytoplasm volume ratio, lipofuscin and neutral lipid accumulation). Additive and synergistic effects were also observed on the expression of estrogen-responsive genes (GSTπ, catalase and 5-HTR) evaluated by RT-Q-PCR. The use of a 1.7K cDNA Mytilus microarray showed that CHP, E2 and CHP/E2, induced 81, 44, and 65 Differentially Expressed Genes (DEGs), respectively. 24 genes were exclusively shared between CHP and CHP/E2, only 2 genes between E2 and CHP/E2. Moreover, 36 genes were uniquely modulated by CHP/E2. Gene ontology annotation was used to elucidate the putative mechanisms involved in the responses elicited by different treatments. Conclusions: The results show complex interactions between CHP and E2 in mussel digestive gland, indicating that the combination of certain pesticides and hormones may give rise to unexpected effects at the molecular/cellular level. Overall, these data demonstrate that CHP can interfere with the mussel responses to natural estrogens. Four-condition experiment. Dual color competitive hybridizations. Common reference (vehicle treated animals, 0.02% Dimethyl sulfoxide, injected with 50 μl of a solution of Artificial Sea Water containing 0.05 % ethanol); Pools of six animals. Biological replicates: 4 controls, 4 Chlorpyrifos, 4 17β-estradiol, 4 Chlorpyrifos-17β-stradiol. One replicate per array.
2011-12-31 | E-GEOD-26222 | biostudies-arrayexpress
Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2.
2014-01-20 | GSE45271 | GEO
Project description:The general objective of this study was to investigate the effects of glabridin in Ishikawa cells in comparison to 17β-oestradiol by studying its mechanism of action via Affymetrix GeneChip® PrimeViewTM array The treatments were the unctreated control, 10µM glabridin, 100nM glabridin, 1nM 17β-E2 and the combination treatment of 1nM 17β-E2 with 100nM glabridin. The cells were treated for 72 hours and the RNA were extracted for microarray and RT-qPCR study.
2015-04-29 | E-GEOD-68333 | biostudies-arrayexpress
Project description:To identify key genes in the early sex development of zebrafish, we generated zebrafish (AB strain) feminized by sex hormone 17β-estradiol (E2, CAS: 50-28-2, 100 ng/L) and masculinized by aromatase inhibitor exemestane (EM, CAS: 107868-30-4, 10 μg/L), and detected their transcriptomes by RNA-seq.
2022-05-11 | GSE126039 | GEO
Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2. Three biological replicates (MASE2 tumours grown in SCID mice, see growth protocol) were analyzed for both conditions of addition of E2 or placebo.
2014-01-20 | E-GEOD-45271 | biostudies-arrayexpress
Project description:17β-HSD1 expression modulates T47D transcript profile in in steroid-deprived medium. The enzyme specifically regulates apoptosis and cancer-related genes in T47D cells cultured in steroid-deprived medium. Genes that primarily involved in Cell cycle progression, such as the Cyclin A2 gene, CCNA2, are generally down-regulated whereas most genes involved in apoptosis and cell death, such as the proapoptotic gene XAF1 and FGF12, are on the contrary up-regulated by 17β-HSD1 knockdown, and 21% of the modulated genes belong to this latter functional category. This correborates with its role previously shown in increasing breast cancer cell proliferation (Aka et al, 2010) and indicates that in addition to its direct role as cell proliferation via incresing E2 and decreasing DHT, 17β-HSD1 may also be involved in oncogenesis by favoring its anti-apoptosis pathway in breast cancer cells 17β-HSD1 may also be involved in oncogenesis by favoring anti-apoptosis pathway and/or inhibiting cell survival pathway. We tested the ability of estrogen to induce or repress endogenous genes of T47D by microarray analysis. A total of 131 genes were found to increase or decrease 1.5-fold or higher in response to 17 beta-estradiol (1 nM for 48 h). Besides, the gene regulation occuring in steroid-deprived conditions showed that 17β-HSD1 modulates gene expression in steroid-independent manners. Our study thus demonstrates that 17β-HSD1 modulates the E2-independent transcription of endogenous genes in T47D cells. The E2-dependent transcription as well as the E2-independent transcription are significantly modulated by 17β-HSD1 in breast cancer cells We first report here that breast cancer cell transcript profile is independtly modulated by both 17β-HSD1 and its principale product estradiol.
2016-09-01 | GSE77345 | GEO
Project description:Estradiol-17β (E2) has been shown to promote primordial follicle (PF) formation and to involve BMP2 as a downstream effector to promote PF in the hamsters. However, the molecular mechanism whereby these factors regulate ovarian somatic cells to pre-granulosa cells (preGC) transition leading to PF formation remains unclear. The objective of this study was to determine whether BMP2 and/or E2 would regulate the expression of specific ovarian transcriptome during preGC transition and PF formation in the mouse ovary. BMP2 mRNA level increased during the period of PF formation with concurrent presence of BMP2 protein in ovarian somatic cells. E2 but not BMP2 exposure led to increased expression of ovarian BMP2 mRNA, and the effect of E2 could not be suppressed by LDN 193189 (LDN). Either BMP2 or E2 stimulated PF formation without inducing apoptosis. RNAseq analysis of ovaries exposed to exogenous BMP2 or E2 revealed differential expression of several thousand genes. Most of the differentially expressed genes (DEG), which were common between BMP2 or E2 treatment demonstrated concordant changes, reinforcing the idea of cooperativity between E2 and BMP2 during PF formation. Further, we have Identified E2, in cooperation with BMP2, could affect the expression of three major transcription factors GATA2, GATA4 and EGR2 and one serine protease, hepsin in preGC during PF formation. Taken together, results of this study suggest that E2 and BMP2 may regulate ovarian gene expression that promote somatic cells to preGC transition and PF formation in the mouse ovary.
2022-05-31 | GSE197122 | GEO
Project description:Five ovariectomized (OVX) Brown Norway rats (Charles Rivers Laboratories, Wilmington, DE, USA) weighing 200-250 g received 10 µL of 17β-estradiol (E2) eye drops once daily in both eyes for three weeks [20]. The eye drops contained 0.1% (w/v) E2 in saline vehicle containing 20% (w/v) 2-hydroxypropyl-β-cyclodextrin. Five OVX control rats received 10 µL of this vehicle as eye drops for the same dosing regimen and duration. After 24 h of the last treatment, the animals were euthanized by CO2 overexposure, and their eyes were immediately enucleated followed by the isolation of the retina. The tissue samples were rinsed with saline and, then, blotted dry for preparation to label-free shotgun proteomic analyses. All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee at the University of North Texas Health Science Center before the initiation of the studies (approval number: 2018-0028). Directions to sample names CF1: Control (female) retina sample #1 CF2: Control (female) retina sample #2 CF3: Control (female) retina sample #3 CF4: Control (female) retina sample #4 CF5: Control (female) retina sample #5 EF1: E2-treated (female) retina sample #1 EF2: E2-treated (female) retina sample #2 EF3: E2-treated (female) retina sample #3 EF4: E2-treated (female) retina sample #4 EF5: E2-treated (female) retina sample #5
2020-05-27 | PXD010851 | Pride