E-GEOD-52399
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA227779
PROVIDER: E-GEOD-52399 | ExpressionAtlas | 2015-07-29
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:In the present study, to identify potential paracrine factor for the stromal regulation of E2-induced epithelial cell proliferation, we treated epithelial and stromal cell populations of mouse uterine primary co-culture with either oil or E2. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 119 genes and down-regulation of 28 genes in epithelial cell populations and up-regulation of 144 genes and down-regulation of 192 genes in stromal cell population. We analyzed whole gnenome transcription from epithelial and stromal cell populations of mouse uterine primary co-culture using the Affymetrix GeneChip® Mouse Gene 1.0 ST Array (vehicle vs. E2). 3 replicates were performed.
2013-11-15 | E-GEOD-52399 | biostudies-arrayexpress
Project description:In the present study, to identify potential paracrine factor for the stromal regulation of E2-induced epithelial cell proliferation, we treated epithelial and stromal cell populations of mouse uterine primary co-culture with either oil or E2. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 119 genes and down-regulation of 28 genes in epithelial cell populations and up-regulation of 144 genes and down-regulation of 192 genes in stromal cell population.
2013-11-15 | GSE52399 | GEO
Project description:Affymetrix gene chip analysis for the whole mouse genome transcripts of epithelial and stromal cells from mouse uterine primary co-culture treated with either vehicle or E2
| PRJNA227779 | ENA
Project description:Gene expression profiling of hormone treated normal and endometriosis stromal fibroblast cells (eSF). We used Affymetrix Human Gene 1.0 ST arrays. Samples include 4 normal of no uterine pathology (NUP), 4 endometriosis stage I, 4 endometriosis stage IV samples, each treated with Estrogen (E2), Progesterone (P4), E2+P4, or vehicle (veh), for a total of 48 samples on the Affymetrix platform.
2020-02-21 | GSE145701 | GEO
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
2012-04-08 | E-GEOD-36455 | biostudies-arrayexpress
Project description:Genome-wide DNA methylation profiling of hormone treated normal and endometriosis stromal fibroblast cells (eSF). The Illumina Infinium Methylation BeadChip array 450 (HM450) was used. Samples include 4 normal of no uterine pathology (NUP), 4 endometriosis stage I, 4 endometriosis stage IV samples, each treated with Estrogen (E2), Progesterone (P4), E2+P4, or vehicle (veh), for a total of 48 samples analyzed on HM450.
2020-02-22 | GSE130028 | GEO
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.
2012-04-09 | GSE36455 | GEO
Project description:Insulin-like growth factor 1 (IGF1) is primarily synthesized in and secreted from the liver; however, estrogen (E2), through E2 receptor α (ERα), increases uterine Igf1 mRNA levels. Previous ChIP-Seq analyses of the murine uterus have revealed a potential enhancer region distal from the Igf1 transcription start site (TSS) with multiple E2-dependent ERα-binding regions. Here, we show E2-dependent super enhancer–associated characteristics and suggest contact between the distal enhancer and the Igf1 TSS. We hypothesized that this distal super-enhancer region controls E2-responsive induction of uterine Igf1 transcripts. We deleted 430 bp, encompassing one of the ERα-binding sites, thereby disrupting interactions of the enhancer with gene-regulatory factors. As a result, E2-mediated induction of mouse uterine Igf1 mRNA is completely eliminated, whereas hepatic Igf1 expression remains unaffected. This highlights the central role of a distal enhancer in the assembly of the factors necessary for E2-dependent interaction with the Igf1 TSS and induction of uterus-specific Igf1 transcription. Of note, loss of the enhancer did not affect fertility or uterine growth responses. Deletion of uterine Igf1 in a PgrCre;Igf1f/f model decreased female fertility, but did not impact the E2-induced uterine growth response. Moreover, E2-dependent activation of uterine IGF1 signaling was not impaired by disrupting the distal enhancer or by deleting the coding transcript. This indicated a role for systemic IGF1, suggested that other growth mediators drive uterine response to E2, and that uterine-derived IGF1 is essential for reproductive success. Our findings elucidate the role of a super enhancer in Igf1 regulation and uterine growth.
2019-05-08 | GSE125972 | GEO
Project description:Uterine glands and, by inference, their secretions impact uterine receptivity, blastocyst implantation, stromal cell decidualization, and placental development. Changes in gland function across the menstrual cycle are impacted by steroid hormones, estrogen and progesterone, as well as stroma-derived factors. Using an endometrial epithelial organoid (EEO) system, transcriptome and proteome analyses identified distinct responses of the EEO to steroid hormones and prostaglandin E2 (PGE2). Notably, steroid hormones and PGE2 modulated the basolateral secretion of EEO proteins, where cystatin C (CST3) was significantly increased by progesterone and PGE2. CST3 treatment of decidualizing stromal cells significantly decreased the decidualization markers PRL and IGFBP1. The attenuation of stromal cell decidualization via CST3 suggests a role for uterine gland-derived proteins in controlling the extent of decidualization. These findings provide evidence that uterine gland-derived factors directly impact stromal cell decidualization, which has strong implications for better understanding pregnancy establishment and female fertility in humans.
2023-10-11 | PXD034357 | Pride
Project description:ChIP-seq from mice with DNA binding mutations in Esr1 (KIKO mouse). Estrogen Receptor M-NM-1 (ERM-NM-1) interacts with DNA, directly, or indirectly via other transcription factors, referred to as M-bM-^@M-^\tetheringM-bM-^@M-^]. Evidence for tethering is based on in vitro studies and a widely used M-bM-^@M-^\KIKOM-bM-^@M-^] mouse model containing mutations that prevent direct estrogen response element (ERE) DNA-binding. KIKO mice are infertile, due in part to the inability of estrogen (E2) to induce uterine epithelial proliferation. To elucidate the molecular events that prevent KIKO uterine growth, regulation of the pro-proliferative E2 target gene Klf4, and of Klf15, a progesterone (P4) target gene that opposes KLF4M-bM-^@M-^Ys pro-proliferative activity, were evaluated. Klf4 induction was impaired in KIKO uteri; however, Klf15 was induced by E2 rather than by P4. Whole uterine ChIP-seq revealed enrichment of KIKO ERM-NM-1 binding to hormone response elements (HRE), motifs. KIKO binding to HRE motifs was verified using reporter gene and DNA-binding assays. Because the KIKO ERM-NM-1 has HRE DNA-binding activity, we evaluated the M-bM-^@M-^\EAAEM-bM-^@M-^] ERM-NM-1, which has more severe DBD mutations, and demonstrated lack of ERE or HRE reporter gene induction or DNA binding. The EAAE mouse has an ERM-NM-1-null like phenotype, with impaired uterine growth and transcriptional activity. Our findings demonstrate that the KIKO mouse model, which has been used by numerous investigators, cannot be used to establish biological functions for ERM-NM-1 tethering, as KIKO ERM-NM-1 effectively stimulates transcription using HRE motifs. The EAAE-ERM-NM-1 DBD mutant mouse demonstrates that ERM-NM-1 DNA-binding is crucial for biological and transcriptional processes in reproductive tissues, and that ERM-NM-1-tethering may not contribute to estrogen-responsiveness in vivo. 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
2014-04-03 | E-GEOD-56466 | biostudies-arrayexpress