Name: Expression data from ethanol and saline exposed mice [mRNA]
Keywords: transcription profiling by array

OmicsDI

Browse
Submit Data
Databases
API
Help
Login

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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.

OTHER RELATED OMICS DATASETS IN: GSE66646PRJNA277538PRJNA261293PRJNA277534PRJNA290890PRJNA277537

ORGANISM(S): Mus musculus

SUBMITTER: Eric Jonathon Diehl Shiva M Singh

PROVIDER: E-GEOD-66644 | ArrayExpress | 2015-03-07

SECONDARY ACCESSION(S): GSE66644PRJNA277538

REPOSITORIES: GEO, ArrayExpress

ACCESS DATA

Json Xml

Dataset's files

Source:

primary

			Action	DRS
	E-GEOD-66644.idf.txt	Idf
	E-GEOD-66644.processed.1.zip	Processed
	E-GEOD-66644.raw.1.zip	Raw
	E-GEOD-66644.sdrf.txt	Txt

Items per page:

1 - 4 of 4

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

Similar Datasets

brain expression data from adult mice exposed to ethanol at postnatal day 4 and 7

Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the long-term (postnatal day 60 young adult) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis. We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 60 that occur due to ethanol treatment at postnatal days 4 and 7 (synaptogenesis). To generate samples, C57BL/6J pups were injected with ethanol (experimental) or saline (control) at postnatal days 4 and 7. Pups were weaned at postnatal day 25 and sacrificed at postnatal day 60. Total RNA was extracted from whole brain tissue and RNA from three male mice from three different litters were pooled as one biological replicate. Each male ethanol-treated mouse represented in a sample was matched by a control littermate present in a control sample. This study consists of two biological replicates for each experimental group (total mice used was n=12).

2011-12-20 | E-GEOD-34549 | ArrayExpress

Whole brain expression data from postnatal day 7-aged mice exposed to ethanol at postnatal day 7

Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the acute (4h post-treatment) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis (postnatal day 7). We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 7 that occur due to ethanol treatment at postnatal day 7 (synaptogenesis). To generate samples, C57BL/6J pups were injected with ethanol (experimental) or saline (control) at postnatal day 7 (2 x 2.5 g/kg at 0h and 2h). Pups were sacrificed 4 hours following the initial injection. Total RNA was extracted from whole brain tissue and RNA from three male mice from three different litters were pooled as one biological replicate. Each male ethanol-treated mouse represented in a sample was matched by a control littermate present in a control sample. This study consists of two experimental (ethanol-treated) biological replicates and four control (saline vehicle-treated) replicates (total mice used was n=18).

2014-07-18 | E-GEOD-59512 | ArrayExpress

Gene expression profile of adult male offspring from ethanol-consuming mice

Project description:Moderate alcohol consumption during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse moder of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear. We used two independent microarray experiments and focused on the genes identified by both to evaluate the genome-wide alterations to the adult brain transcriptome caused by prenatal ethanol exposure via moderate maternal drinking. To generate samples, two independent groups of female C57BL/6J mice were given access to 10% ethanol in water or water only. Control females had access to water only. Females were mated and continued to drink from gestational day 0 to pup postnatal day 10. Whole brain RNA from adult (postnatal day 70) male ethanol-exposed offspring was extracted. For experiment 1, RNA samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice). For experiment 2, RNA from two mice were pooled per chip and three arrays per treatment were used (3 control, 3 ethanol, total n=12 mice).

2011-12-10 | E-GEOD-34305 | ArrayExpress

MeDIP-chip of adult mouse hippocampus exposed to neonatal ethanol

Project description:In this experiment, we exposed mice to ethanol injections on postnatal days 4 and 7. We then extracted whole-hippocampus on postnatal day 70. We performed MeDIP-chip using an antibody against 5mC. We also perfomed MEDME anaylsis using a chip with fully methylated DNA to act as a control. We found alterations in both modifications at many sites, including oxidative stress genes and imprinted loci. We also found many affect lipid metabolism pathways. Comparision of neonatal ethanol-injected with saline injected C57BL/6J mouse hippocampus in adulthood (day 70)

2015-07-25 | E-GEOD-71313 | ArrayExpress

Expression data from ethanol and saline exposed mice [mRNA]

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. Overall design: 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 | GSE66644 | GEO

Transcription profiling by array of mouse brain after treatment with ethanol

Project description:Moderate alcohol exposure during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse model of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear. We used a microarray experiment and focused on the genes identified by both to evaluate the genome-wide alterations to the adult brain transcriptome caused by prenatal ethanol exposure. To generate samples, female C57BL/6J mice were given ethanol injections (2.5g/kg of ethanol in saline) twice on gestational days 8 and 11 to produce acute ethanol exposure effects. Control females were injected with the same volume of saline. Females were mated. Whole brain RNA from adult (postnatal day 70) male ethanol-exposed offspring was extracted. RNA samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice).

2011-12-16 | E-GEOD-34469 | ArrayExpress

Microarray analysis of Wild-type vs. Brpf1-deficient P4 mouse brain

Project description:RNA was isolated from three pairs of wild-type and Brpf1-deficient mouse brains (the dorsal cortex part) at postnatal day 4 for microarray analysis. The cDNA samples were then labeled and mixed for hybridization with one array. The data from three arrays were obtained and used for bioinformatic analysis.

2015-04-08 | E-GEOD-63909 | ArrayExpress

Expression data from ethanol and saline exposed mice [miRNA]

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. Overall design: Mice were injected with 2.5 g/kg twice on each of posnatal 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 | GSE66645 | GEO

CB1R regulates CDK5 signaling and epigenetically controls Rac1 expression contributing to neurobehavioral abnormalities in mice postnatally exposed to ethanol.

Project description:Fetal alcohol spectrum disorders (FASD) represent a wide array of defects that arise from ethanol exposure during development. However, the underlying molecular mechanisms are limited. In the current report, we aimed to further evaluate the cannabinoid receptor type 1 (CB1R)-mediated mechanisms in a postnatal ethanol-exposed animal model. We report that the exposure of postnatal day 7 (P7) mice to ethanol generates p25, a CDK5-activating peptide, in a time- and CB1R-dependent manner in the hippocampus and neocortex brain regions. Pharmacological inhibition of CDK5 activity before ethanol exposure prevented accumulation of cleaved caspase-3 (CC3) and hyperphosphorylated tau (PHF1) (a marker for neurodegeneration) in neonatal mice and reversed cAMP response element-binding protein (CREB) activation and activity-regulated cytoskeleton-associated protein (Arc) expression. We also found that postnatal ethanol exposure caused a loss of RhoGTPase-related, Rac1, gene expression in a CB1R and CDK5 activity-dependent manner, which persisted to adulthood. Our epigenetic analysis of the Rac1 gene promoter suggested that persistent suppression of Rac1 expression is mediated by enhanced histone H3 lysine 9 dimethylation (H3K9me2), a repressive chromatin state, via G9a recruitment. The inhibition of CDK5/p25 activity before postnatal ethanol exposure rescued CREB activation, Arc, chromatin remodeling and Rac1 expression, spatial memory, and long-term potentiation (LTP) abnormalities in adult mice. Together, these findings propose that the postnatal ethanol-induced CB1R-mediated activation of CDK5 suppresses Arc and Rac1 expression in the mouse brain and is responsible for persistent synaptic plasticity and learning and memory defects in adult mice. This CB1R-mediated activation of CDK5 signaling during active synaptic development may slow down the maturation of synaptic circuits and may cause neurobehavioral defects, as found in this FASD animal model.

2019-01-01 | S-EPMC6333777 | BioStudies

Neonatal Ethanol Disturbs the Normal Maturation of Parvalbumin Interneurons Surrounded by Subsets of Perineuronal Nets in the Cerebral Cortex: Partial Reversal by Lithium.

Project description:Reduction in parvalbumin-positive (PV+) interneurons is observed in adult mice exposed to ethanol at postnatal day 7 (P7), a late gestation fetal alcohol spectrum disorder model. To evaluate whether PV+ cells are lost, or PV expression is reduced, we quantified PV+ and associated perineuronal net (PNN)+ cell densities in barrel cortex. While PNN+ cell density was not reduced by P7 ethanol, PV cell density decreased by 25% at P90 with no decrease at P14. PNN+ cells in controls were virtually all PV+, whereas more than 20% lacked PV in ethanol-treated adult animals. P7 ethanol caused immediate apoptosis in 10% of GFP+ cells in G42 mice, which express GFP in a subset of PV+ cells, and GFP+ cell density decreased by 60% at P90 without reduction at P14. The ethanol effect on PV+ cell density was attenuated by lithium treatment at P7 or at P14-28. Thus, reduced PV+ cell density may be caused by disrupted cell maturation, in addition to acute apoptosis. This effect may be regionally specific: in the dentate gyrus, P7 ethanol reduced PV+ cell density by 70% at P14 and both PV+ and PNN+ cell densities by 50% at P90, and delayed lithium did not alleviate ethanol's effect.

2019-01-01 | S-EPMC6418394 | BioStudies