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
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.
Project description:Using microarray technology, we compared the global expression pattern of uterine RNA from ovariectomized control mice to those of ovariectomized mice treated with estradiol for various intervals between 30 minutes and 24 hours. Keywords: estrogen, uterus, genomic, mouse
Project description:To examine the effect of E2 treatment for the miRNA expression, at 15 week old, female wiled type mice were ovariectomized, and after one week, estradiol (E2) was delivered at a concentration of 0.050 mg/kg body weight/day. 24 hours after chemical treatment, uteruses from mice treated with or without E2 were dissected.
Project description:The ovarian hormones estrogen and progesterone orchestrate the transcriptional programs required to direct functions of the uterus for initiation and maintenance of pregnancy. Estrogen, acting via estrogen receptor alpha (ERα), regulates gene expression by activating and repressing distinct genes involved in signaling pathways that regulate cellular and physiological responses including cell division, water influx, and immune cell recruitment. Historically, these transcriptional responses have been postulated to reflect a biphasic physiological response. In this study, we explored the transcriptional responses of the ovariectomized mouse uterus to 17β-estradiol (E2) by RNA-seq to obtain global expression profiles of protein coding transcripts (mRNAs) and long noncoding RNAs (lncRNAs) following 0.5, 1, 2 and 6 hours of treatment. The E2-regulated mRNA and lncRNA expression profiles in the mouse uterus indicate an association between lncRNAs and mRNAs that regulate E2-driven pathways and reproductive phenotypes in the mouse. The transient E2-regulated transcriptome is reflected in the time-dependent shifting of biological processes regulated in the uterus in response to E2. Moreover, high expression of some conserved lncRNAs that are E2-regulated in the mouse uterus are predictive of low overall survival in endometrial carcinoma patients (e.g., H19, KCNQ1OT1, MIR17HG, and FTX). Collectively, this study (1) describes a genomic approach for identifying E2-regulated lncRNAs that may serve critical function in the uterus and (2) provides new insights into our understanding of the regulation of hormone-regulated transcriptional responses with implications in pregnancy and endometrial pathologies.
Project description:To examine the effect of E2 treatment for the miRNA expression, at 15 week old, female wiled type mice were ovariectomized, and after one week, estradiol (E2) was delivered at a concentration of 0.050 mg/kg body weight/day. 24 hours after chemical treatment, uteruses from mice treated with or without E2 were dissected. Two group experiment (WT-OVX and WT-OVX-E2) three replicates per condition
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.
Project description:Estrogen induce organ-specific cell proliferation and development in female reproductive organs, though the reproductive differentiation, sex maturation, implantation and lactation. However, the mechanism of organ-specific estrogen responsive genes is unknown. Thus, we examined early estrogen responsive genes in mouse uterus, vagina and mammary gland. Keywords: organ specificity 70-day-old ovariectomized mice (C57BL/6J)(n=4) were treated with 17beta-estradiol (5micro g/kg) or sesame oil. Whole uterus (Ut), vagina (Vg) and mammary gland (Mg) were sacrificed 6h after the injection.
Project description:Examination of crosstalk between Aryl hydrocarbonreceptor (AHR) and Estrogen receptor (ER) in tha rat uterus on the level of miRNA transcriptome The study was designed to see the overall ncRNA-expression change in the uterus induced by E2