Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from ethanol and saline exposed mice [mRNA]

ABSTRACT: Mouse models of Fetal Alcohol Spectrum Disorder can be used to assess molecular changes underlying the disorder. Neonatal ethanol exposure in mice can be used to model third trimester ethanol exposure in humans. Mice were injected with 2.5 g/kg twice on each of postnatal days 4 and 7. Mice were allowed to reach postnatal day 70, at which time whole-hippocampus was isolated and snap frozen. Tissue was thawed and RNA was isolated. RNA run on affymetrix gene expression array according to standard protocol. Each array was a pool of three mice, for a total n=9 ethanol-exposed and 9 control mice. All mice were male.

ORGANISM(S): Mus musculus

SUBMITTER: Eric Diehl

PROVIDER: E-GEOD-66644 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Alteration of Gene Expression, DNA Methylation, and Histone Methylation in Free Radical Scavenging Networks in Adult Mouse Hippocampus following Fetal Alcohol Exposure.

Chater-Diehl Eric J EJ Laufer Benjamin I BI Castellani Christina A CA Alberry Bonnie L BL Singh Shiva M SM

PloS one 20160502 5

The molecular basis of Fetal Alcohol Spectrum Disorders (FASD) is poorly understood; however, epigenetic and gene expression changes have been implicated. We have developed a mouse model of FASD characterized by learning and memory impairment and persistent gene expression changes. Epigenetic marks may maintain expression changes over a mouse's lifetime, an area few have explored. Here, mice were injected with saline or ethanol on postnatal days four and seven. At 70 days of age gene expression ...[more]

PMID: 27136348

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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. Experiment Overall Design: There were 3 DES doses (1, 10 and 1000 ug/kg/day) administered to neonates on days 1-5. RNA was pooled for 10 mice, with each dose having its own matching control (corn oil). Dye-flipped hybridizations were performed for each paired comparison.

Dataset Information

Expression data from ethanol and saline exposed mice [mRNA]

Publications

Alteration of Gene Expression, DNA Methylation, and Histone Methylation in Free Radical Scavenging Networks in Adult Mouse Hippocampus following Fetal Alcohol Exposure.

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