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Gene expression changes in uteri of mice treated with 17beta-estradiol (E2), p-Phenoxyphenol (PhOP), or p-pentyloxyphenol (PeOP)

ABSTRACT: Gene expression changes in uteri of mice treated with 17beta-estradiol (E2), p-Phenoxyphenol (PhOP), or p-pentyloxyphenol (PeOP)

PROVIDER: PRJNA635278 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11853676_1.fastq.gz	Fastqsanger.gz
	SRR11853676_2.fastq.gz	Fastqsanger.gz
	SRR11853677_1.fastq.gz	Fastqsanger.gz
	SRR11853677_2.fastq.gz	Fastqsanger.gz
	SRR11853678_1.fastq.gz	Fastqsanger.gz

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Gene expression changes in uteri of mice treated with 17beta-estradiol (E2), p-Phenoxyphenol (PhOP), or p-pentyloxyphenol (PeOP)

Project description:p-Phenoxyphenol (PhOP) and p-pentyloxyphenol (PeOP) have been reported to be estrogenic in vitro. But their in vivo estrogenic activities have rarely been of concern. In this study, we performed an immature mouse uterotrophic assay and next-generation transcriptome sequencing (RNA-seq) to study the estrogenicity of PhOP and PeOP, as well as E2.

2020-05-28 | GSE151242 | GEO

Gene expression signatures in uteri from nuclear and membrane effects of Estradiol on Estrogen receptor ERÎ±

Project description:To further study gene expression regulated by 17b-estradiol in uteri, we have employed whole gene microarray profiling to identify genes specifically regulated by the Estrogen receptor ERÎ± localized either at the plasma membrane or in the nucleus. Two mice models have been used, the mice named ERa-AF2Â° (named AF2_KO and on C57BL6/J background) in which 7 aminoacids have been deleted in the AF2 domain and the mice C451A-ERa (named MISS_KO and on C57BL6/N background) mutated for the C451 into Ala on ERa. Control littermates were used for each mutant mice respectively name AF2_WT or MISS_WT. 17b-estradiol induced gene expression in uteri from ovariectomized mice was measured after 6 hours exposure to 0 (PLB) and 8Âµg/kg of 17b-estradiol (E2) injected subcutaneously in castor oil.

2014-07-01 | E-GEOD-53237 | biostudies-arrayexpress

Transcription profiling of uteri from mice treated with 17beta-estradiol for different durations to study the molecular mechanism for estrogen induced uterine growth.

Project description:Immature (19/20 days of age) Alpk:APfCD-1 mice were treated with arachis oil (AO) vehicle or 0.4mg/kg 17beta-estradiol (E2), via a single subcutaneous injection, and sacrificed at 1hr, 2hr, 4hr, 8hr, 24hr, 48hr, 72hr post dose.

2007-09-22 | E-GEOD-2195 | biostudies-arrayexpress

Transcription profiling of uteri from gonadectomized C57BL/6 mice injected with 17-Estradiol (E2) to identify genes modulated by a physiological dose of E2 in uterus.

Project description:17Ã-Estradiol (E2) is well known to be associated with uterine cancer, endometriosis, and leiomyomas. Although insulin-like growth factor I (IGF-I) has been identified as a mediator of the uterotrophic effect of E2 in several studies, this mechanism is still not well understood. In the present study, identification of the genes modulated by a physiological dose of E2, in the uterus, has been done in ovariectomized mice using Affymetrix microarrays. The E2-induced genomic profile shows that multiple genes belonging to the IGF-I pathway are affected after exposure to E2. Two phases of regulation could be identified. First, from 0 to 6 h, the expression of genes involved in the cell cycle, growth factors, protein tyrosine phosphatases, and MAPK phosphatases is quickly upregulated by E2, while IGF-I receptor and several genes of the MAPK and phosphatidylinositol 3-kinase pathways are downregulated. Later, i.e., from 6 to 24 h, transporters and peptidases/proteases are stimulated, whereas defense-related genes are differentially regulated by E2. Finally, cytoarchitectural genes are modulated later. The present data show that a physiological dose of E2 induces, within 24 h, a series of transcriptional events that promote the uterotrophic effect. Among these, the E2-mediated activation of the IGF-I pathway seems to play a pivotal role in the uterotrophic effect. Furthermore, the protein tyrosine phosphatases and MAPK phosphatases are likely to modulate the estrogenic uterotrophic action by targeting, at different steps, the IGF-I pathway. Experiment Overall Design: Ten 10-11 weeks old C57Bl/6 mice were gonadectomized under isoflurane-induced anesthesia and sacrified seven days after GDX. Mice were injected s.c with E2 (0.05ug/mice) or vehicle, at 0.5, 1, 3, 6, 12 or 24 h before sacrifice. Uteri was removed and pooled before total RNA extraction. Samples was hybridized to U74Av2 Genechips (Affymetrix).

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Transcription profiling by array of uteruses from immature Alpk:APfCD-1 mice treated with arachis oil vehicle (AO), 17beta-estradiol (E2), or genistein (GEN) to study the effects of E2 and GEN on gene expression.

Project description:Immature (19/20 days of age) Alpk:APfCD-1 mice were treated with arachis oil (AO) vehicle, 0.4mg/kg 17beta-estradiol (E2), or 250mg/kg genistein (GEN), via a single subcutaneous injection, and sacrificed at 1hr, 2hr, 4hr, 8hr, 24hr, 48hr, 72hr post dose.

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Transcription profiling of uteruses from Alpk:APfCD-1 mice treated with arachis oil (AO) vehicle, 17beta-estradiol (E2), diethylstilbestrol (DES), or genistein (GEN) to study the effects of E2, GEN, and DES on gene transcription.

Project description:Three independent replicates of 4 groups of immature (19/20 days of age) Alpk:APfCD-1 mice were treated with arachis oil (AO) vehicle, 2.5ug/kg 17beta-estradiol (E2), 2ug/kg diethylstilbestrol (DES), or 50mg/kg genistein (GEN), via 3 daily subcutaneous injection, and sacrificed 72hr after initial dose.

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Gene expression signatures in uteri from WT and Arg260-ERα mice in response to E2

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Project description:Gene expression changes in uteri of mice treated with 17beta-estradiol (E2), p-Phenoxyphenol (PhOP), or p-pentyloxyphenol (PeOP)

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Equivalence of biologic responses induced in the mouse uterus by E2, GEN, and DES

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