Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE66646
PROVIDER: PRJNA261293 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MeDIP of adult whole brain tissue from fetal alcohol exposed mice
| PRJNA203646 | ENA
Project description:Background Maternal consumption of alcohol during pregnancy is associated with a range of physical, cognitive and behavioural outcomes in the offspring which are collectively called fetal alcohol spectrum disorders. We and others have proposed that epigenetic modifications, such as DNA methylation and post-translational histone modifications, mediate the effects of prenatal alcohol exposure on gene expression and, ultimately, phenotype. Here we use an inbred C57BL/6J mouse model of early gestational ethanol exposure equivalent, developmentally, to the first 3-4 weeks of pregnancy in humans to examine the long-term effects on gene expression and epigenetic state in the hippocampus. Results Gene expression analysis in the hippocampus revealed sex- and age-specific up-regulation of solute carrier family 17 member 6 (Slc17a6), which encodes vesicular glutamate transporter 2 (VGLUT2). Transcriptional up-regulation correlated with decreased DNA methylation and enrichment of histone H3 lysine 4 trimethylation, an active chromatin mark, at the Slc17a6 promoter. In contrast to Slc17a6 mRNA levels, hippocampal VGLUT2 protein levels were significantly decreased in adult ethanol-exposed offspring, suggesting an additional level of post-transcriptional control. MicroRNA expression profiling in the hippocampus identified four ethanol-sensitive microRNAs, of which miR-467b-5p was predicted to target Slc17a6. In vitro reporter assays showed that miR-467b-5p specifically interacted with the 3’ UTR of Slc17a6, suggesting that it contributes to the reduction of hippocampal VGLUT2 in vivo. A significant correlation between microRNA expression in the hippocampus and serum of ethanol-exposed offspring was also observed. Conclusions Prenatal ethanol exposure has complex transcriptional and post-transcriptional effects on Slc17a6 (VGLUT2) expression in the mouse hippocampus. These effects are observed following a relatively moderate exposure that is restricted to early pregnancy, modelling human consumption of alcohol before pregnancy is confirmed, and are only apparent in male offspring in adulthood. We propose that altered epigenetic and microRNA-mediated regulation of glutamate neurotransmission in the hippocampus contributes to the cognitive and behavioural phenotypes observed in fetal alcohol spectrum disorders. Our findings also support the idea that circulating microRNAs could be used as biomarkers of early gestational ethanol exposure and/or hippocampal dysfunction.
2015-10-09 | GSE60000 | GEO
Project description:To assess gene expression underlying alcohol memory in different regions of the brain, we performed total RNA-sequencing (RNA-seq) on brain tissue (prefrontal cortex or dorsal hippocampus) from C57BL/6 adult mice that had undergone alcohol placement conditioning and either placed back into alcohol context (retrieval, Ret) or briefly handled as a control (no retrieval, NoRet)
2023-03-07 | GSE205586 | GEO
Project description: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.
2015-03-07 | E-GEOD-66644 | biostudies-arrayexpress
Project description:MeDIP-chip of adult mouse hippocampus exposed to neonatal ethanol
| PRJNA290890 | ENA
Project description:In this report we assessed alterations to adult mouse brain tissue by assaying DNA cytosine methylation and small noncoding RNA (ncRNA) expression, specifically the microRNA (miRNA) and small nucleolar RNA (snoRNA) subtypes. We found long lasting alterations in DNA methylation as a result of fetal alcohol exposure, specifically in the imprinted regions of the genome harboring ncRNAs and sequences interacting with regulatory proteins. ~20% of the altered ncRNAs mapped to three imprinted regions: Snrpn-Ube3a, Dlk1-Dio3, and Sfmbt2, which showed differential methylation and have been previously implicated in neurodevelopmental disorders. The findings of this report help to expand on the mechanisms behind the long lasting changes in the brain transcriptome of FASD individuals. Comparison of fetal alcohol exposed and matched control adult C57/BL6J mice brains with olfactory bulbs removed
2013-05-21 | E-GEOD-47111 | biostudies-arrayexpress
Project description:Exposure to alcohol during early embryonic or fetal development has been linked with a variety of adverse outcomes, the most common of which are structural and functional abnormalities of the central nervous system. Behavioral and cognitive deficits reported in individuals exposed to alcohol in utero include intellectual impairment, learning and memory difficulties, diminished executive functioning, attention problems, poor motor function and hyperactivity. The economic and social costs of these outcomes are substantial and profound. Improvement of neurobehavioural outcomes following prenatal alcohol exposure requires greater understanding of the mechanisms of alcohol-induced damage to the brain. Here we use a mouse model of relatively moderate ethanol exposure early in pregnancy and profile gene expression in the hippocampus and caudate putamen of adult male offspring. The effects of offspring sex and age on ethanol-sensitive hippocampal gene expression were also examined.
2016-10-20 | GSE87703 | GEO
Project description:Exposure to alcohol during early embryonic or fetal development has been linked with a variety of adverse outcomes, the most common of which are structural and functional abnormalities of the central nervous system. Behavioral and cognitive deficits reported in individuals exposed to alcohol in utero include intellectual impairment, learning and memory difficulties, diminished executive functioning, attention problems, poor motor function and hyperactivity. The economic and social costs of these outcomes are substantial and profound. Improvement of neurobehavioural outcomes following prenatal alcohol exposure requires greater understanding of the mechanisms of alcohol-induced damage to the brain. Here we use a mouse model of relatively moderate ethanol exposure early in pregnancy and profile gene expression in the hippocampus and caudate putamen of adult male offspring. The effects of offspring sex and age on ethanol-sensitive hippocampal gene expression were also examined.
2016-10-20 | GSE87700 | GEO
Project description:Exposure to alcohol during early embryonic or fetal development has been linked with a variety of adverse outcomes, the most common of which are structural and functional abnormalities of the central nervous system. Behavioral and cognitive deficits reported in individuals exposed to alcohol in utero include intellectual impairment, learning and memory difficulties, diminished executive functioning, attention problems, poor motor function and hyperactivity. The economic and social costs of these outcomes are substantial and profound. Improvement of neurobehavioural outcomes following prenatal alcohol exposure requires greater understanding of the mechanisms of alcohol-induced damage to the brain. Here we use a mouse model of relatively moderate ethanol exposure early in pregnancy and profile gene expression in the hippocampus and caudate putamen of adult male offspring. The effects of offspring sex and age on ethanol-sensitive hippocampal gene expression were also examined.
2016-10-20 | GSE87699 | GEO
Project description:Purpose: The transcriptional alterations underlying physological changes in fetal alcohol spectrum disorder are largely unidentified. Here we perform RNA sequencing on control and embryonic alcohol exposed (EAE/FAE) zebrafish at larval (13 dpf) and adult stages in order to identify significant transcriptional alterations under normal and HFHC diet conditions.
2020-12-01 | GSE142311 | GEO