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Analysis of mRNA transcriptomic changes in ethanol-exposed human embryonic stem cell (hESC)-derived cortical interneurons using ribosome depletion RNA sequencing

ABSTRACT: Purpose: The goal of this study to use ethanol-exposed human embryonic stem cell (hESC)-derived neural cells as models to investigate mRNA 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 mRNA sequencing. The sequence reads were processed using the RNA-seq processing pipeline Pipeliner [Front Genet. 2019; 10:614] workflow. Ethanol-induced mRNA transcriptomic changes were analyzed by the Limma-Voom method. Results: When the significance level was set at FC>2.0 & P<0.01, 19 coding genes showed differential expression, and all of them were downregulated after a 7-day ethanol exposure. Conclusions: The hESC-derived neural cell model study can partially validate mRNA transcriptomic changes in postmortem brains of subjects with alcohol use disorder.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181049 | GEO | 2021/10/13

REPOSITORIES: GEO

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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.

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2021-10-13 | GSE181813 | GEO

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2021-10-13 | GSE181804 | GEO

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Project description:Purpose: The goal of this study to examine mRNA transcriptomic changes in reward-related brain regions of subjects with alcohol use disorder. Methods: Total RNAs were extracted from postmortem caudate nucleus of 12 AUD and 12 control subjects. rRNA depletion RNA sequencing was performed and the sequence reads were processed using the bulk RNA-seq processing pipeline Pipeliner workflow (Federico et al. Front Genet 2019; 10, 614). AUD-associated mRNA transcriptomic changes were analyzed by the Limma-Voom method. Results: Differentially expressed mRNAs (absolute FC>2.0 & P<0.05) were identified in postmortem caudate nucleus of subjects with alcohol use disorder (AUD). Chronic alcohol consumption may alter mRNA transcriptome profiles in reward-related brain regions, resulting in alcohol-induced neuroadaptations.

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Transcriptional alterations in cycling neural stem cells underlying alcohol use disorders

Project description:Ethanol inhibits the proliferation of neural stem cells in the fetal, adolescent, and adult brain. The consequences are cognitive deficits associated with fetal alcohol spectrum disorder and alcohol use disorder. We tested the hypothesis that ethanol affects progression through cell cycle checkpoints by differentially modifying transcriptional processes. Monolayer cultures of NS-5 neural stem cells were treated for 48 hr with the mitogenic agent FGF2 or the anti-mitogenic TGFβ1 in the absence or presence of ethanol. Cell cycle elongation was induced by a global down-regulation of genes involved in cell cycle progression, including the cyclin E system. Checkpoint regulation occurred downstream of p21 and Jun-oncogene signaling cascades. Thus, ethanol can affect cell cycle progression by altering transcript expression of strategic genes downstream of the G1/S checkpoint.

2010-04-01 | GSE19436 | GEO

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