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Transcription profiling by array of mouse oviduct, uterus and vagina treated with DES from new born mice to understand the mechanism of the differentiation of female reproductive tracts

ABSTRACT: Diethylstilbestrol (DES) inhibits the differentiation of female reproductive tracts during fetal and neonatal days . We examined global gene expressions in the oviduct, uterus and vagina in newborn mice with or without DES. These results suggest understanding the mechanism of the differentiation of female reproductive tracts. Keywords: ordered

ORGANISM(S): Mus musculus

SUBMITTER: Atsuko Suzuki

PROVIDER: E-GEOD-1886 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression change in the Müllerian duct of the mouse fetus exposed to diethylstilbestrol in utero.

Suzuki Atsuko A Urushitani Hiroshi H Sato Tomomi T Kobayashi Tomohiro T Watanabe Hajime H Ohta Yasuhiko Y Iguchi Taisen T

Experimental biology and medicine (Maywood, N.J.) 20070401 4

In utero exposure to diethylstilbestrol (DES) induces various abnormalities in the Müllerian duct of the mouse. In order to understand the underlying molecular mechanisms associated with DES-induced abnormalities of the Müllerian duct, gene expression was examined on Gestation Day (GD) 19 in mouse fetuses exposed to DES (67 microg/kg body weight) from GDs 10 to 18. Microarray analysis revealed that 387, 387, and 225 genes were upregulated and 177, 172, and 75 genes were downregulated by DES in t ...[more]

PMID: 17392486

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Murine Müllrian duct Day0 DES

Project description:Diethylstilbestrol (DES) inhibits the differentiation of female reproductive tracts during fetal and neonatal days . We examined global gene expressions in the oviduct, uterus and vagina in newborn mice with or without DES. These results suggest understanding the mechanism of the differentiation of female reproductive tracts. Keywords: ordered

2004-10-28 | GSE1886 | GEO

Gene expression profiling in the seminal vesicles (SVs) from neonatal DES-treated mice [array]

Project description:DES is a synthetic estrogen that is associated with adverse effects on reproductive organs. Our group has employed estrogen receptor (ER) α knockout (αERKO) mice to gain insight into the contribution of ER-dependent pathways in mediating the effects of neonatal DES exposure in female and male reproductive tract tissues. The objective of this study is to compare gene expression profiles between the WT-veh and -DES groups or αERKO-veh and -DES from the adult male mice (week 10) of the SV tissues to identify differential genes.

2018-03-27 | GSE95314 | GEO

Genome-wide transcriptome in the mouse seminal vesicles (SVs) and uterus (U) following neonatal DES exposure

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Genome-wide transcriptome in the mouse seminal vesicles (SVs) and uterus (U) following neonatal DES exposure [RNA-seq]

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DNA methylation profiling by MBD-Seq in the mouse seminal vesicles (SVs) and uterus (U) following neonatal DES exposure

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Histone H3K27ac modification profiling by ChIP-Seq in the mouse seminal vesicles (SVs) and uterus (U) following neonatal DES exposure

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Expression data from the reproductive tracts of WT, Hoxa9,10,11, and Hoxd9,10,11 mutant mice

Project description:Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition, we observed a surprising anti-dogmatic posteriorization of the uterine epithelium. Reproductive tracts were collected from WT and Hox mutant mice (n=3/genotype) aged 3-7 months in order to characterize the molecular changes caused by mutation of Hoxa9,10,11 and Hoxd9,10,11. Female mice were staged and collected in diestrus.

2013-08-01 | E-GEOD-41993 | biostudies-arrayexpress

Developmental Exposure to DES Alters Uterine Gene Expression That Maybe Associated with Neoplasia Later in Life

Project description:Previously, we described a mouse model where the well-known reproductive carcinogen, diethylstilbestrol (DES), caused uterine adenocarcinoma following neonatal treatment. Tumor incidence was dose-dependent reaching >90% by 18 mo. following 1000 µg/kg/day of DES. These tumors followed the initiation/promotion model of hormonal carcinogenesis with developmental exposure as the initiator, and exposure to ovarian hormones at puberty as the promoter. To identify molecular pathways involved in DES-initiation events, uterine gene expression profiles were examined in prepubertal mice exposed to DES (1, 10 or 1000 µg/kg/day) on days 1-5 and compared to age-matched controls. Of more than 20,000 transcripts, approximately 3% were differentially expressed in at least one DES treatment group compared to controls; several transcripts demonstrated dose-responsiveness. Assessment of gene ontology annotation revealed alterations in genes associated with cell growth, differentiation, and adhesion. When expression profiles were compared to published studies of uteri from 5 day old DES-treated mice, or adult mice treated with 17β estradiol, similarities were seen suggesting persistent differential expression of estrogen responsive genes following developmental DES exposure. Moreover, several significantly altered genes have been identified in human uterine adenocarcinomas. Four altered genes [Lactotransferrin (Ltf), Transforming growth factor beta inducible (Tgfβ1), Cyclin D1 (Ccnd1), and Secreted frizzled-related protein 4 (Sfrp4)], selected for real time RT-PCR analysis, correlated well with the directionality of the microarray data. These data suggest altered gene expression profiles observed two weeks after treatment ceased, were imprinted at the time of developmental exposure and maybe related to the initiation events resulting in carcinogenesis. Keywords: dose reponse

2007-06-14 | GSE5825 | GEO

RNA-Seq expression data from the reproductive tracts of WT, Hoxa91011, and Hoxd91011 mutant mice

Project description:Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition we observed a surprising anti-dogmatic posteriorization of the uterine epithelium. Reproductive tracts were collected from WT and Hox mutant mice (n=3/genotype) aged 3-7 months in order to characterize the molecular changes caused by mutation of Hoxa9,10,11 and Hoxd9,10,11. Female mice were staged and collected in diestrus.

2013-08-01 | E-GEOD-42339 | biostudies-arrayexpress

Postmating transcriptional changes in reproductive tracts of con- and heterospecifically-mated Drosophila mojavensis females

Project description:In internally fertilizing organisms, mating involves a series of highly coordinated molecular interactions between the sexes that occur within the female reproductive tract. In species with promiscuous mating systems, traits involved in postcopulatory interactions are expected to evolve rapidly, potentially leading to postmating-prezygotic (PMPZ) reproductive isolation between diverging populations. Here, we use a novel study design to investigate the postmating transcriptional response of Drosophila mojavensis female reproductive tracts following copulation with either conspecific or heterospecific (D. arizonae) males at three time points postmating. Relatively few genes (15 total) were transcriptionally regulated in the female lower reproductive tract in response to conspecific mating. Heterospecifically-mated females exhibited significant perturbations in the expression of the majority of these genes, and also downregulated transcription of a number of others, including several involved in mitochondrial function. These striking regulatory differences indicate failed postcopulatory molecular interactions between the sexes consistent with the strong PMPZ isolation observed for this cross. We also report, for the first time, the transfer of male mRNA transcripts to females during copulation. These included transcripts from male accessory-gland proteins (ACPs), a finding with potentially broad implications for understanding postcopulatory molecular interactions between the sexes. Dataset from Postmating transcriptional changes in reproductive tracts of con- and heterospecifically-mated Drosophila mojavensis females Bono, JM, Matzkin,LM, Kelleher, ES, and Markow, MA, Proceedings of the National Academy of Sciences, USA.

2012-01-01 | GSE27454 | GEO

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