Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153625 | ENA |
REPOSITORIES: ENA
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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: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: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:Analysis of transcriptome of tissue recombinants (mouse seminal vesicle epithelial [SVE] cells or prostate epithelial [PE] cells, and rat urogenital sinus [UGS] mesenchymal cells) grown under the kidney capsule in athymic nude mice for 3 months.
2016-06-24 | GSE81432 | GEO
Project description:We isolated fetal murine urogenital sinus epithelium and urogenital sinus mesenchyme and determined their global gene expression profiles to define their differentially expressed regulators. To distinguish gene expression patterns that are shared by other developing epithelial/mesenchymal compartments in the embryo from those that pertain to the prostate stem cell niche, we also determine the global gene expression of epidermis and dermis of the same embryos. We identified a distinctive core of transcripts that were differentially regulated in the prostate stem cell niche. Our analysis indicates that several of the key transcriptional components that are likely to be active in the embryonic prostate stem cell niche regulate processes such as self-renewal (e.g., E2f and Ap2), lipid metabolism (e.g., Serbp1) and cell migration (e.g., Areb6 and Rreb1). Several of the promoter binding motifs that are enriched in the profiles are shared between the prostate epithelial/mesenchymal compartments and their epidermis/dermis counterparts, indicating their likely relevance in epithelial/mesenchymal signaling in primitive cellular compartments. We also focused on defining ligand-receptor interactions that may be relevant in controlling signals in the stem cell niche and identified the Wnt/beta-catenin, ephrin, Notch, sonic hedgehog, FGF, TGF-beta and bone morphogenic signaling pathways as being of likely relevance in the prostate stem cell niches. Members of the integrins family including those that bind extracellular matrix proteins such as laminin and activate latent TGF-beta are also expressed in the prostate niche.development. Keywords: Differential gene expression Six biological replicate experiments were performed for UGE. Five biological replicate experiments were performed for UGM. Four biological replicate experiments were performed for Epidermis. Four biological replicate experiments were performed for Dermis.
2010-08-29 | E-GEOD-17797 | biostudies-arrayexpress
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: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
2018-12-31 | GSE121086 | GEO
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.
2010-12-06 | GSE24928 | 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:Expression data from estradiol-treated fetal urogenital sinus mesenchyme cells
| PRJNA117555 | ENA