Estren Behaves as a Weak Estrogen Rather than a Non-genomic Selective Activator in the Mouse Uterus
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE4615 | GEO | 2006/04/07
SECONDARY ACCESSION(S): PRJNA95323
REPOSITORIES: GEO
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Project description:A proposed membrane-mediated mechanism of rapid non genomic response to estrogen has been the intense focus of recent research. Estren (Es), a synthetic steroid, is reported to act selectively through a rapid membrane-mediated pathway, rather than through the classical nuclear estrogen receptor (ER)-mediated pathway, to maintain bone density in ovaierectomized mice without uterotropic effects. To further evaluate the mechanism and physiological effects of Es we studied responses in adult ovariectomized mice. Experiment Overall Design: Mice were treated with sesame oil vehicle (Sigma), E2 (Steraloids; 1 µg/mouse) estren (300 µg/mouse), or dihydrotestosterone (DHT, Steraloids; 50 µg/mouse) and uteri were collected 2 or 24 hours after treatment and snap frozen in liquid nitrogen. Three or four uteri from each treatment group were pooled and RNA was prepared using Trizol reagent (Invitrogen, Carlsbad CA) and the RNeasy clean up protocol (Qiagen Valencia CA). Gene expression profiling was conducted using Agilent Mouse Oligo arrays with ~20,000 genes represented (Agilent Technologies, Palo Alto, CA). Five hundred ng of total RNA was amplified and labeled using the Agilent Low RNA Input Fluorescent Linear Amplification Kit according to manufacturer's protocol. For each two color comparison, 750 ng of each Cy3- and Cy5-labeled cRNA were mixed and fragmented using the Agilent In Situ Hybridization Kit protocol. Hybridizations were performed for 17 hours in a rotating hybridization oven according to the Agilent 60-mer oligo microarray processing protocol prior to washing and scanning with an Agilent Scanner (Agilent Technologies, Wilmington, DE). Each sample pair was hybridized on 2 replicate chips. Experiment Overall Design: Data was obtained using the Agilent Feature Extraction software (v7.5, v8.1), using defaults for all parameters.
2008-06-22 | E-GEOD-4615 | biostudies-arrayexpress
Project description:Females were ovariectomized and injected with saline estradiol or estriol. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray compare ealry and late responses to a potent and a weak estrogen agaonist.
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Project description:Females were ovariectomized and injected with saline estradiol or estriol. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray compare ealry and late responses to a potent and a weak estrogen agaonist. 3 uteri per group were analyzed individually on one-color Agilent arrays.
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Project description:This SuperSeries is composed of the following subset Series: GSE13858: Global survey of miRNA microarray of uterus, ovariectomized female mice with or without estrogen (E2) treatment GSE13859: Global survey of miRNA microarray of whole embryo, wild type vs estrogen receptor alpha knockout mice Refer to individual Series
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Project description:Membrane estrogen receptor (ER) alpha stimulates AMP kinase to suppress SREBP1 processing and lipids in liver Here we present evidence that signaling from membrane-localized ERalpha similarly suppresses a subset of mRNAs in the livers of female WT and membrane only estrogen receptor (MOER) transgenic mice but not in estrogen receptor knock out (ERKO) mice Three month old wild type, MOER and ERKO mice were ovariectomized and utilized per IRB-approved. Following ovariectomy and recovery the animals were injected intraperitoneally with PPT (100 ?g) or oil placebo (0.1 mL) daily for 3 days. Whole livers were removed upon euthanasia.
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Project description:Estrogen rescues the loss of gas exchange units in ovariectomized mice. This project studies the mechanisms of this rescue in ovariectomized mice treated with or without estrogen. Keywords: other
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Project description:There are concerns regarding possible reproductive toxicity from consumption of soy including an increased risk of endometriosis and endometrial cancer. We used global uterine gene expression profiles in adult ovariectomized (OVX) female rats assessed by RNAseq to examine the estrogenicity of soy protein isolate (SPI) and the potential for feeding SPI to alter estrogen signaling in the uterus. Rats were fed AIN93G diets made with casein (CAS) or SPI from postnatal day (PND) 30. Rats were OVX on PND 50 and infused with 17 beta-estradiol (E2) or vehicle. E2 increased uterine wet weight (P<0.05) and significantly altered expression of 2084 uterine genes. In contrast, SPI feeding had no effect on uterine weight and only altered expression of 177 genes. Overlap between E2 and SPI genes was limited to 69 genes (3%). GO analysis indicated significant differences in uterine biological processes affected by E2 and SPI and little evidence for recruitment of ER alpha to the promoters of ER-responsive genes after SPI feeding. The major E2 up-regulated uterine pathways were cancer pathways and extracellular organization. SPI feeding up-regulated uterine PPAR signaling and fatty acid metabolism. The combination of E2 and SPI feeding resulted in significant regulation of 715 fewer genes relative to E2 alone. In a separate experiment, the combination of E2 and SPI reversed the ability of E2 to induce uterine proliferation in response to the carcinogen dimethybenz(a)anthracene (DMBA). These data suggest SPI does not act as a weak estrogen in the uterus but appears to be a selective estrogen receptor modulator (SERM) interacting with a small sub-set of E2-regulated genes and to be anti-estrogenic in the presence of endogenous estrogens. Rat uterus mRNA of ovariectomized adult female rats subject to four different diets (Caseine, Caseine + E2, Soy and Soy+E2 ) were sequenced, in triplicate, in an Illumina GAIIx sequencer.
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Project description:The uterus, a female reproductive organ regulated by the sex hormones estrogen and progesterone, undergoes periodic cyclical changes. The estrous cycle refers to the reproductive cycle in non-primate mammalian females. During the mouse estrous cycle, the uterus undergoes various physiological changes as a result of dynamic hormonal changes. Accurate regulation of these changes is crucial for the establishment of a successful pregnancy. Notably, estrogen plays an important role in the regulation of the proestrus and estrus stages of the estrous cycle. Family with sequence similarity 3 (Fam3) is a cytokine-like gene family with four members: Fam3a, Fam3b, Fam3c, and Fam3d. Expression and regulation of the Fam3 family members in mouse uterine physiology remain largely unknown. Therefore, this study aimed to investigate the expression of Fam family members in the uterus during the estrous cycle and evaluate its regulation by estrogen using a mouse model. Analysis of mouse uterine RNA sequencing data revealed upregulated expression of Fam3b, Fam3c, and Fam3d during the proestrus and estrus stages. Fam3d expression was dynamically regulated during the estrous cycle, with high expression levels during the proestrus and estrus stages. To investigate whether Fam3d expression is regulated by estrogen, we administered estradiol (E2) to ovariectomized mice at different time points. Fam3d expression was highest 24 h after E2 injection, suggesting that estrogen plays a crucial role in regulating Fam3d expression. Furthermore, inhibition experiments using the estrogen receptor alpha (ERα) antagonist ICI revealed that estrogen regulates Fam3d expression through the ERα-mediated pathway. Immunofluorescence staining demonstrated that FAM3D was exclusively expressed in the luminal and glandular epithelia but not in the stroma. Additionally, FAM3D was predominantly localized in the cytoplasm, particularly in the apical region, and not in the nucleus. These findings provide valuable insights into the potential role of Fam3d in the uterus and lay the groundwork for future research on its function and significance in uterine physiology.
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Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERα and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERα binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERα, and that ERα binding is increased by E2. Approximately 15% of the uterine ERα binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERα binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERα binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERα to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERα bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERα binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERα and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues.
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Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERM-NM-1 and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERM-NM-1 binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERM-NM-1, and that ERM-NM-1 binding is increased by E2. Approximately 15% of the uterine ERM-NM-1 binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERM-NM-1 binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERM-NM-1 binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERM-NM-1 to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERM-NM-1 bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERM-NM-1 binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERM-NM-1 and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues. one sample each, vehicle ER-alpha ChIP seq,1 hour estradiol ER-alpha ChIP seq, vehicle RNA polymerase II ChIP seq,1 hour estradiol RNA polymerase II ChIP seq, input DNA
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