MRNA and miRNA expression analysis of developmental ethanol exposure in zebrafish
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ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE30497 | GEO | 2011/10/01
SECONDARY ACCESSION(S): PRJNA143351
REPOSITORIES: GEO
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Project description:During early neurogenesis, multiple whole animal gene expression profiling studies revealed widespread changes in developmental mRNA and miRNA abundance in ethanol-exposed embryos. Consistent with a role for miRNAs in neurobehavioral development, miRNA target prediction analyses identified multiple miRNAs misexpressed in the ethanol exposed cohorts that were also predicted to target inversely expressed transcripts known to influence brain morphogenesis. [mRNA] A twelve chip study using total RNA recovered from pools of 75 tropical 5D zebrafish embryos at 24 hours post fertilization (hpf). Embryos were exposed to control embryo medium, 100 mM ethanol, or 300 mM ethanol from 4-24 hpf, with four-fold biological redundancy per condition. A single 12x135K Nimblegen array was used to measure the expression level of 38,489 genes from Danio rerio using 60-mer probes, with three-fold technical redundancy. [miRNA] A twelve chip study using miRNA recovered from pools of 75 tropical 5D zebrafish embryos at 12, 24, 36, and 48 hours post fertilization (hpf). Embryos were exposed to control embryo medium or 300 mM ethanol from 4-24 hpf, with two-fold biological redundancy per condition. Control samples were pooled and hybridized to a single array. 12 miRZebrafish arrays (based on MirBase release 12.0) were used to measure the expression level of 218 mature miRNA from Danio rerio, with 12-fold technical redundancy.
2011-09-30 | E-GEOD-30497 | biostudies-arrayexpress
Project description:Prenatal exposure to ethanol leads to a myriad of developmental disorders known as fetal alcohol spectrum disorder, often characterized by growth and mental retardation, central nervous system damage and specific craniofacial dysmorphic features. Although the exact mechanisms of ethanol toxicity are not well understood it is known that ethanol exposure during development affects the expression of several genes involved in cell cycle control, apoptosis and transcription. MicroRNAs (miRNAs) are implicated in some of these processes however it is unclear if they are involved in ethanol-induced toxicity. Here we tested whether ethanol deregulates miRNA expression in zebrafish embryos and if a miRNA deregulation signature could be inferred. For this, zebrafish embryos were exposed to two different ethanol concentrations (1% and 1.5%) from 4 hours post-fertilization (hpf) to 24hpf. MicroRNA expression profiles revealed that ethanol exposure induces deregulation of miRNA expression significantly. Seven miRNAs are commonly up-regulated after both ethanol treatments, namely miR-153a, miR-725, miR-30d, let-7k, miR-100, miR-738 and miR-732, whereas downregulation of miR-23a, miR-203, let-7c, miR-128 and miR-193b is detected after 1% ethanol exposure only. Target prediction of deregulated miRNAs shows that putative targets are involved in cell cycle control, apoptosis and transcription, which are the main processes affected by ethanol toxicity. The overall study shows that the effects of ethanol on miRNA deregulation are dose-dependent and that miRNAs are relevant in the context of alcohol toxicity. Moreover, a miRNA toxicity signature for embryonic ethanol exposure was obtained.
2012-06-18 | GSE32632 | GEO
Project description:Prenatal exposure to ethanol leads to a myriad of developmental disorders known as fetal alcohol spectrum disorder, often characterized by growth and mental retardation, central nervous system damage and specific craniofacial dysmorphic features. Although the exact mechanisms of ethanol toxicity are not well understood it is known that ethanol exposure during development affects the expression of several genes involved in cell cycle control, apoptosis and transcription. MicroRNAs (miRNAs) are implicated in some of these processes however it is unclear if they are involved in ethanol-induced toxicity. Here we tested whether ethanol deregulates miRNA expression in zebrafish embryos and if a miRNA deregulation signature could be inferred. For this, zebrafish embryos were exposed to two different ethanol concentrations (1% and 1.5%) from 4 hours post-fertilization (hpf) to 24hpf. MicroRNA expression profiles revealed that ethanol exposure induces deregulation of miRNA expression significantly. Seven miRNAs are commonly up-regulated after both ethanol treatments, namely miR-153a, miR-725, miR-30d, let-7k, miR-100, miR-738 and miR-732, whereas downregulation of miR-23a, miR-203, let-7c, miR-128 and miR-193b is detected after 1% ethanol exposure only. Target prediction of deregulated miRNAs shows that putative targets are involved in cell cycle control, apoptosis and transcription, which are the main processes affected by ethanol toxicity. The overall study shows that the effects of ethanol on miRNA deregulation are dose-dependent and that miRNAs are relevant in the context of alcohol toxicity. Moreover, a miRNA toxicity signature for embryonic ethanol exposure was obtained. Zebrafish embryos were obtained from spawning adults in groups of about 10 males and 10 females. Zebrafish embryos were collected and Petri dishes with approximately 250 eggs each were incubated at 28M-BM-:C to allow normal zebrafish development until 4hpf, when blastula is reached. At this stage, embryos were examined under a dissecting microscope and those that had developed normally were selected for EtOH exposure (approximately 200 eggs). Briefly, 200 embryos were randomly distributed into plastic Petri dishes containing 20 mL of EtOH test solutions (1% EtOH, 1.5% EtOH). All solutions were made by dilution of absolute EtOH in system water. Exposure was from 4hpf to 24hpf. At this stage, solutions were changed by system water and embryos were allowed to grow until 24hpf. The control group was allowed to grow in plain system water. Zebrafish embryos were collected at 24hpf for microarray analysis. Two biological replicates were performed for each assay.
2012-06-17 | E-GEOD-32632 | biostudies-arrayexpress
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure. A total of 48 Rat ST Gene 1.0 GeneChips and 48 miRNA 2.0 GeneChips were run on RNA purified from 2 brain regions (amygdala and ventral striatum) of postnatal day 42 Long Evans rats. 3 replicate arrays were run for each gender within 4 different treatment groups (prenatal ethanol or prenatal saline exposed; postnatal socially-enriched or non-enriched environment)
2014-08-28 | E-GEOD-60819 | biostudies-arrayexpress
Project description:Purpose: The goal of this study to use ethanol-exposed human embryonic stem cell (hESC)-derived neural cells as models to investigate microRNA expression changes in the brains of subjects with alcohol use disorder (AUD). Methods: hESCs were differentiated into neural cells (mainly cortical interneurons), which were then cultured in media with or without ethanol (50-100 mM) for 7 days (by duplicate experiments). Total RNAs were extracted from hESC-derived neural cells (with or without ethanol exposure) for small RNA sequencing. The sequence reads were processed using the Comprehensive Analysis Pipeline for miRNA Sequencing Data (CAP-miRseq) workflow. Ethanol-induced miRNA transcriptomic changes were analyzed by the Limma-Voom method. Results: A 7-day ethanol exposure led to differential expression of six miRNAs (absolute FC>2.0 & P<0.05) in hESC-derived cortical interneurons. Three miRNAs were upregulated (>2-fold increase & P<0.05), while three other miRNAs were downregulated (> 2-fold decrease & P < 0.05) due to ethanol exposure. Conclusions: The hESC-derived neural cell model study can partially validate miRNA transcriptomic changes in postmortem brains of subjects with alcohol use disorder.
2021-10-13 | GSE181050 | GEO
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure.
2014-08-28 | GSE60819 | GEO
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure.
2014-08-29 | GSE60900 | GEO
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure. A total of 48 samples were analyzed by small RNA-Sequencing using RNA purified from 2 brain regions (amygdala and ventral striatum) of postnatal day 42 Long Evans rats. 3 replicate sequencing runs were performed for each gender within 4 different treatment groups (prenatal ethanol or prenatal saline exposed; postnatal socially-enriched or non-enriched environment)
2014-08-29 | E-GEOD-60900 | biostudies-arrayexpress
Project description:We conducted a preliminary investigation to determine whether ethanol-induced alterations in placental gene expression may have some utility as a diagnostic indicator of maternal drinking during pregnancy as well as a prognostic indicator of risk for adverse neurobehavioral outcomes in affected offspring.
2010-01-29 | GSE18162 | GEO
Project description:We conducted a preliminary investigation to determine whether ethanol-induced alterations in placental gene expression may have some utility as a diagnostic indicator of maternal drinking during pregnancy as well as a prognostic indicator of risk for adverse neurobehavioral outcomes in affected offspring. Pregnant Long-Evans rats voluntarily consumed either a 0% or 5% ethanol solution four hours each day throughout gestation. Ethanol consumption produced a mean maternal daily intermittent peak serum ethanol concentration of 84 mg/dL. Placentas were harvested on Gestational Day 20 for gene expression studies.
2010-02-21 | E-GEOD-18162 | biostudies-arrayexpress