Testosterone- and estrogen-induced genes in urogenital sinus mesenchyme
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: William Ricke
PROVIDER: E-GEOD-37620 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The goal of this experiment was to determine if testosterone (T) and estradiol-17 beta (E2) induced gene expression in mouse urogenital sinus mesenchymal (UGM) cells. When UGM grown in culture was treated with T+E2, numerous genes were increased and decreased compared to untreated controls. Quantitative RT-PCR was used to verify results of a subset of genes.
2012-04-27 | GSE37620 | GEO
Project description:Developmental estrogen exposure causes permanent alterations to mouse prostate development. Fetal prostatic mesenchyme cells regulate epithelial cell proliferation and differentiation, and alterations to mesenchymal regulation of prostate epithelial cell proliferation and differentiation may lead to permanent changes in gland structure and function. Our goal was to understand how mesenchymal cells convert estrogen signaling to stimuli that affect epithelial cells. We used microarrays to identify estrogen-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells.
2009-06-27 | GSE16854 | GEO
Project description:Developmental estrogen exposure causes permanent alterations to mouse prostate development. Fetal prostatic mesenchyme cells regulate epithelial cell proliferation and differentiation, and alterations to mesenchymal regulation of prostate epithelial cell proliferation and differentiation may lead to permanent changes in gland structure and function. Our goal was to understand how mesenchymal cells convert estrogen signaling to stimuli that affect epithelial cells. We used microarrays to identify estrogen-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells. Experiment Overall Design: Urogenital sinus mesenchymal cells were obtained from CD-1 male mouse fetuses at gestation day 17 and cultured in the presence of 0.1 μM estradiol .
2009-07-05 | E-GEOD-16854 | biostudies-arrayexpress
Project description:Stem cell enrichment provides a tool to examine prostate stem cells obtained from benign and malignant tissue. Functional assays can enrich stem cells based on common stem cell phenotypes, such as high ATP binding cassette (ABC) transporter mediated efflux of Hoechst substrates (side population assay). This functional assay is based upon mechanisms that protect cells from environmental insult thus contributing to the survival and protection of the stem cell population. We have isolated and analyzed cells digested from twelve clinical prostate specimens based on the side population assay. Prostate stem cell properties of the isolated cells were tested by serial recombination with rat urogenital mesenchyme. Recombinants with side population cells demonstrate an increase in the frequency of human ductal growth and the number of glands per recombinant when compared to recombinants with non-side population cells. Isolated cells were capable of prostatic growth for up to three generations in the recombination assay with as little as 125 sorted prostate cells. The ability to reproducibly use cells isolated by fluorescence activated cell sorting from human prostate tissue is an essential step to a better understanding of human prostate stem cell biology. ABC transporter G2 (ABCG2) was expressed in recombinants from side population cells indicating the side population cells have self-renewal properties. Epithelial cell differentiation of recombinants was determined by immunohistochemical analysis for expression of the basal, luminal, and neuroendocrine markers, p63, androgen receptor, prostate specific antigen, and chromogranin A, respectively. Thus, the ABCG2 expressing side population demonstrates multipotency and self-renewal properties indicating stem cells are within this population.
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Project description:Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), is a well-known, ubiquitous estrogenic chemical. To investigate the effects of fetal exposure to low-dose BPA on the development of the prostate, we first examined the alterations of in situ sex steroid hormonal environment in the mouse urogenital sinus (UGS). Next, to investigate the BPA-specific gene alterations related to increases of the E2 levels and aromatase activity, we performed comprehensive gene expression analysis using Affymetrix GeneChip in the BPA-treated or DES-treated male UGS at embryonic day 17th and postnatal day 1st.
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Project description:Developmental exposure of mouse fetuses to estrogens results in dose-dependent permanent effects on prostate morphology and function. Fetal prostatic mesenchyme cells express estrogen receptor alpha (ERα) and androgen receptors and convert stimuli from estrogens and androgens into signaling to regulate epithelial cell proliferation and differentiation. To obtain mechanistic insight into the role of different doses of estradiol (E2) in regulating mesenchymal cells, we examined E2-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells. Urogenital sinus mesenchyme cells were obtained from male mouse fetuses at gestation day 17 and exposed to 10 pM, 100 pM or 100 nM E2 in the presence of a physiological concentration of dihydrotestosterone (0.69 nM) for four days. Gene ontology studies suggested that low doses of E2 (10 pM and 100 pM) induce genes involved in cell adhesion, morphological tissue development, and sterol biosynthesis but suppress genes involved in growth factor signaling and cell adhesion. Genes showing inverted-U-shape dose responses (enhanced by E2 at 10 pM E2 but suppressed at 100 pM) were identified, and their enrichment in the glycolytic pathway was demonstrated. At the highest dose (100 nM), E2 induced genes enriched not only for cell adhesion but also steroid hormone signaling and metabolism, cytokines and their receptors, cell-to-cell communication, Wnt signaling, and TGF-β signaling. These results suggest that prostate mesenchymal cells may regulate epithelial cells through direct cell contacts when estrogen level is low whereas soluble growth factors might play significant roles when estrogen level is high.
2012-03-21 | GSE36630 | GEO
Project description:Dnmt1 is an important regulator of tissue development and differentiation. To assess the effects of epithelium Dnmt1 deletion in the developing urogenital sinus (precursor of the urethra and prostate in males), we isolated urogenital sinus epithelial tissue from Dnmt1 deleted mouse embryos and wildtype mouse embryos. The transcriptomes were analyzed by RNA-seq
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Project description:Developmental exposure of mouse fetuses to estrogens results in dose-dependent permanent effects on prostate morphology and function. Fetal prostatic mesenchyme cells express estrogen receptor alpha (ERα) and androgen receptors and convert stimuli from estrogens and androgens into signaling to regulate epithelial cell proliferation and differentiation. To obtain mechanistic insight into the role of different doses of estradiol (E2) in regulating mesenchymal cells, we examined E2-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells. Urogenital sinus mesenchyme cells were obtained from male mouse fetuses at gestation day 17 and exposed to 10 pM, 100 pM or 100 nM E2 in the presence of a physiological concentration of dihydrotestosterone (0.69 nM) for four days. Gene ontology studies suggested that low doses of E2 (10 pM and 100 pM) induce genes involved in cell adhesion, morphological tissue development, and sterol biosynthesis but suppress genes involved in growth factor signaling and cell adhesion. Genes showing inverted-U-shape dose responses (enhanced by E2 at 10 pM E2 but suppressed at 100 pM) were identified, and their enrichment in the glycolytic pathway was demonstrated. At the highest dose (100 nM), E2 induced genes enriched not only for cell adhesion but also steroid hormone signaling and metabolism, cytokines and their receptors, cell-to-cell communication, Wnt signaling, and TGF-β signaling. These results suggest that prostate mesenchymal cells may regulate epithelial cells through direct cell contacts when estrogen level is low whereas soluble growth factors might play significant roles when estrogen level is high. Primary culture urogenital sinus mesenchymal cells were isolated from prostate glands of gestation day 17 CD1 male mouse fetuses. Cells were then exposed to 10 pM or 100 pM 17beta-estradiol or vehicle (0.05% ethanol) for four days in the presence of 690 pM 5alpha-dihydrotestosterone. Total cellular RNA was then isolated for determination of transcriptomal profiles by Affymetrix mouse gene 1.0 ST array.
2012-03-21 | E-GEOD-36630 | biostudies-arrayexpress
Project description:Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), is a well-known, ubiquitous estrogenic chemical. To investigate the effects of fetal exposure to low-dose BPA on the development of the prostate, we first examined the alterations of in situ sex steroid hormonal environment in the mouse urogenital sinus (UGS). Next, to investigate the BPA-specific gene alterations related to increases of the E2 levels and aromatase activity, we performed comprehensive gene expression analysis using Affymetrix GeneChip in the BPA-treated or DES-treated male UGS at embryonic day 17th and postnatal day 1st. Pregnant female C57BL/6 mice were exposed to BPA (20 μg/kg/day) or synthetic estrogen Diethylstilbestrol (DES: 0.2 μg/kg/day), which were dissolved in tocopherol-stripped corn oil, on embryonic day 13 (E13) to E16. Between E17 and postnatal day 1 (P1), all animals were terminated by an overdose of isoflurane followed by cervical dislocation. Fetuses were collected at E17, E18, P0, and P1. The bladder and urethra were removed and dissected to isolate UGS and collected in RNA later. To isolate pure UGS, other tissues such as the bladder, urethra, Wolffian duct (WD), seminal vesicle (SV), and Mullerian duct (MD) were removed from both the male and female urogenital tracts. The histopathology of the mouse UGS was then examined by hematoxylin and eosin staining. Total RNA was extracted using the Qiagen mini RNA Easy kit. Each RNAs were linearly amplified and hybridized to Affymetrix GeneChip.
2010-12-06 | E-GEOD-24928 | biostudies-arrayexpress
Project description:Cancer cells differentiate along specific lineages that largely determine their clinical and biologic behavior. Distinct cancer phenotypes from different cells and organs likely result from unique gene expression repertoires established during lineage commitment in the embryo and maintained after malignant transformation. We used comprehensive gene expression analysis to examine this concept in the prostate, an organ with a readily manipulable developmental program and a high propensity for cancer. We focused on gene expression changes in the murine prostate rudiment (Urogenital Sinus, UGS) at three time points during the first 48 hours of exposure to androgen, which initiates proliferation and invasion of prostate epithelial buds into surrounding mesenchyme. Keywords: time course, prostate gland development
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