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Estrogen response uterine gene profile in Ex3αERKO

ABSTRACT: WT and Ex3aERKO females were ovariectomized and injected with saline or estradiol. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray to determine if the Ex3aERKO mice would lack the residual transcritpional resposnes seen in the previous aERKO model.

ORGANISM(S): Mus musculus

PROVIDER: GSE23072 | GEO | 2010/07/23

SECONDARY ACCESSION(S): PRJNA131677

REPOSITORIES: GEO

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Estrogen response uterine gene profile in Ex3αERKO

Project description:WT and Ex3aERKO females were ovariectomized and injected with saline or estradiol. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray to determine if the Ex3aERKO mice would lack the residual transcritpional resposnes seen in the previous aERKO model. 3 uteri per group were analyzed individually on one-color Agilent arrays. Comparisons were made within ERa genotype (WT saline to WT E treated; Ex3aERKO saline to Ex3aERKO E treated)

2010-07-22 | E-GEOD-23072 | biostudies-arrayexpress

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Project description:Uterine tissue is highly responsive to estrogen, which plays a mayor role in sympathetic innervation remodeling in myometrium; Microarrays were used to investigate which estrogen resposive myometrial proteins can be involved in innervation modulation Experiment Overall Design: Mature female rats were ovariectomized, than treated with estradiol benzoate or vechicle, myometrial samples were analyzed 6 or 24 h after treatment

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Peri- and post-pubertal estrogen exposures of female mice optimize uterine responses later in life

Project description:At birth, all female mice, including those that either lack estrogen receptor α (ERα-knockout) or that express mutated forms of ERα (AF2ERKI), have a hypoplastic uterus. However, uterine growth and development that normally accompanies pubertal maturation does not occur in ERα-knockout or AF2ERKI mice, indicating ERα mediated estrogen signaling is essential for this process. Mice that lack Cyp19 (aromatase, ArKO mice), an enzyme critical for estrogen (E2) synthesis, are unable to make E2, and lack pubertal uterine development. A single injection of E2 into ovariectomized adult (10 weeks old) females normally results in uterine epithelial cell proliferation, however, we observe that, although ERα is present in the ArKO uterine cells, no proliferative response is seen. We assessed the impact of exposing ArKO mice to E2 during pubertal and post-pubertal windows and observed that E2 exposed ArKO mice acquired growth responsiveness. Analysis of differential gene expression between unexposed ArKO samples and samples from animals exhibiting the ability to mount an E2-induced uterine growth response (WT or E2 exposed ArKO) revealed activation of EZH2 and HAND2 signaling and inhibition of GLI1 responses. EZH2 and HAND2 are known inhibit uterine growth, and GLI1 is involved in IHH signaling, which is a positive mediator of uterine response. Finally, we show that exposure of ArKO females to dietary phytoestrogens results in their acquisition of uterine growth competence. Altogether our findings suggest that pubertal levels of endogenous and exogenous estrogens impact biological function of uterine cells later in life via ERα-dependent mechanisms. We compared uterine RNA from ovariectomized adult aromatase knockout mice (ARKO) mice that were untreated to WT mice and to ARKO that were administered estradiol benzoate (EB) to induce uterine epithelial cell growth competence

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Uterine gene profiles from WT, KIKO (DNA-binding deficient ERα) and aERKO mice treated with estradiol or xenoestrogens

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24 hour time course: regulation of uterine genes by estradiol in ovariectomized mice

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

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