Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA323484 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3590960.fastq.gz | Fastqsanger.gz | |||
| SRR3590961.fastq.gz | Fastqsanger.gz | |||
| SRR3590962.fastq.gz | Fastqsanger.gz | |||
| SRR3590963.fastq.gz | Fastqsanger.gz | |||
| SRR3590964.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Traditional whole-tissue sequencing approaches do not fully capture brain cell-type specific effects of chronic alcohol. Therefore, the purpose of this study was to identify the specific transcriptome alterations in astrocytes due to chronic alcohol. Methods: We performed RNA-sequencing on astrocytes isolated from the prefrontal cortex (PFC) of C57BL/6J mice following chronic every-other-day alcohol consumption. Results: Differential expression analysis revealed alcohol-induced gene expression changes unique to astrocytes that could not be identified using whole tissue homogenate analysis. Enrichment analysis revealed involvement of calcium-related signaling and regulation of extracellular matrix genes in the astrocyte response to alcohol abuse. Conclusion: Our study presents the first focused analysis on the astrocyte transcriptome following chronic alcohol consumption, provides a framework for studying the functional response of astrocytes to alcohol and the possible astrocyte-specific effects of alcohol. In addition, our data represents a novel resource for groups interested in biological functions of astrocytes in the adult mouse PFC.
2018-01-10 | GSE92457 | GEO
Project description:Chronic and binge ethanol consumption in humans and in animal models has been associated with the induction of injury (such as fibrosis and scarring) in the liver as well as the intestine, brain, lung and immune system. The effects of chronic ethanol consumption on the human kidney are protective as seen in large population studies are controversial with the preponderance of the data suggesting protection less so than injury. The most recent meta-analysis was by Konig et al (2015) who studied 5476 participants aged 28–75 years from the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study to assess associations between alcohol consumption and risk of chronic kidney disease (CKD). They found in this population-based cohort, alcohol consumption was inversely associated with the risk of developing CKD. The protective effects of ethanol on the kidney present a unique model system to develop new hypothesis on protection against end organ damage by fibrosis. The data on the effects of alcohol or alcohol consumption at the molecular level on renal parenchyma are sparse. In cell culture and animal models chronic ethanol exposure has been show to induce protein post-translational modification (acetylation), protein expression (upregulation of cytochrome P450 CYP2E1 and local platelet-activating factor receptor (PAFR) ligand formation) as well as neutrophil infiltration and activation. Since hepatocytes do not express PAFR, these data suggest that the response of the kidney to chronic alcohol consumption is distinct from that of the liver or lung. Therefore, we hypothesized that mechanisms of ethanol-induced renal injury or protection are regulated by a protein signaling networks (PSN) modulated acutely by the phosphoproteome and long term epigenetically by the acetylproteome. To address this hypothesis we have initiated a tiered proteomics study to determine the effects of chronic alcohol consumption on the murine kidney and with a secondary insult of acute exposure of lipopolysaccharide (LPS) on the renal proteome, phosphoproteome and the acetylproteome. Data have already been collected on the total proteome and the phosphoproteome using a multiplexing approach. Data will be collected early spring on the acetylproteome.
2019-05-15 | GSE81947 | GEO
Project description:LncRNAs are important regulators of quantitative and qualitative features of the transcriptome. We have used QTL and other statistical analyses to identify a gene coexpression module associated with the phenotype of alcohol consumption. The “hub gene” of this module, Lrap (Long non-coding RNA for alcohol preference), was an unannotated transcript resembling a lncRNA. We used partial correlation analyses to establish that Lrap is a major contributor to the integrity of the coexpression module. Using CRISPR/Cas9 technology, we disrupted an exon of Lrap in Wistar rats. The genetically modified rats were assessed for alcohol consumption and brain RNA expression levels were evaluated using RNASeq. Measures of alcohol consumption in wild type, heterozygous and knockout rats demonstrated that disruption of Lrap produced increases in alcohol consumption/alcohol preference. The disruption of Lrap also produced changes in expression of over 700 other transcripts. Furthermore, it became apparent that Lrap may have a function in alternative splicing of the affected transcripts. More than 20% of the differentially expressed isoforms exhibited evidence for novel alternative splicing between Lrap+/+ and Lrap-/- rats. The GO category of “Response to Ethanol” emerged as one of the top candidates in an enrichment analysis of the differentially expressed transcripts. We validate the role of Lrap as a mediator of alcohol consumption by rats, and also implicate Lrap as a modifier of the expression and splicing of a large number of brain transcripts. A defined subset of these transcripts significantly impacts alcohol consumption by rats (and possibly humans).
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Project description:We investigated the molecular mechanisms of chronic alcohol consumption or lipopolysaccharide insult by gene expression profiling in prefrontal cortex and liver of C57BL/6J mice. We identified similar patterns of transcriptional changes in brain and liver among three different alcohol consumption tests and lipopolysaccharide injection. We also demonstrated distinct genomic consequences of different types of alcohol consumption. The microarray experiment was performed to compare gene expression changes induced by three separate paradigms of alcohol consumption and immune activation by lipopolysaccharide injection. The three tests of alcohol consumption were the continuous chronic two bottle choice (Chronic), two bottle choice available every other day (Chronic Intermittent) and limited access to one bottle of ethanol (Drinking in the Dark). All alcohol studies utilized 20% ethanol and each treatment group had it's own control group which received only water. The immune activation test consisted of 2 lipopolysaccharide injections (1 mg/kg i.p.) spaced one week apart, with animals being sacrificed one week after the last injection. Control animals received saline injections. All studies used female, adult mice.
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Project description:Chronic alcohol exposure can cause myocardial degenerative diseases, manifested as cardiac insufficiency, arrhythmia, etc. These are defined as alcoholic cardiomyopathy (ACM). Alcohol-mediated myocardial injury has previously been studied through metabolomics, and it has been proved to be involved in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway related to the biosynthesis of unsaturated fatty acids and oxidative phosphorylation, which tentatively explored the mechanism of ACM induced by chronic drinking. To further study the myocardial damage caused by alcohol, the mouse model of ACM successfully established previously was used to perform proteomics analysis on myocardial specimens. Fifty-six differentially expressed proteins (DEPs) were identified, and they are involved in the KEGG pathway related to fatty acid biosynthesis, lipid metabolism, oxidative stress, and the development of dilated cardiomyopathy (DCM). The present study further demonstrated the underlying causes of myocardial damage caused by chronic alcohol consumption and lays the foundation for further research to clarify the underlying mechanism of ACM.
2022-08-12 | PXD032949 | Pride
Project description:We investigated the molecular mechanisms of chronic alcohol consumption or lipopolysaccharide insult by gene expression profiling in prefrontal cortex and liver of C57BL/6J mice. We identified similar patterns of transcriptional changes in brain and liver among three different alcohol consumption tests and lipopolysaccharide injection. We also demonstrated distinct genomic consequences of different types of alcohol consumption.
2013-04-01 | GSE42789 | GEO
Project description:Male rats from one of four strains (Wistar, AA, HAD or P) were housed individually in standard hanging rodent cages (Ehret, Emmendingen, Germany) on a 12-hour light-dark cycle with lights on at 07:00 a.m.. Animals were provided with food (Sniff, Soest, Germany), tap water, 5, 10 and 20% (v/v) ethanol solutions ad libidum for 12 months. Control animals did not receive any alcohol. P rats and HAD rats were provided by Ting-Kai Li, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda. AA rats were provided by Petri Hyytiä and Kalervo Kiianmaa, Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland. To find out which genes are differentially expressed in response to alcohol consumption, we investigated the pancreas of the animals with respect to gene expression in alcohol-drinking and control animals. Animals with the highest alcohol consumption were chosen from a series of rats. We obtained microarray data from pancreatic tissue of these animals by using Affymetrix RG U34A microarrays, which contain probes for 8799 transcripts.
2009-12-31 | E-MEXP-776 | biostudies-arrayexpress
Project description:Accumulating evidence suggests that lifestyle-related factors may influence radiation responses and the resulting cancer risks through epigenetic mechanisms, such as miRNA regulations. Chronic alcohol consumption is a major risk factor for various pathologies, including alcoholic liver disease. We have recently shown that consumption of Japanese sake promotes glutathione metabolism and anti-oxidative activities in the liver of irradiated C57BL/6 mice. Here we show that chronic alcohol consumption resulted in elevated ciculating levels of the inflammatory cytokine TNF-α and that it triggered specific miRNA regulations (such as the upregulation of the radio-resistant miR-210) that are susceptible to influence the resulting radiation effects in the mouse liver.
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Project description:There is a growing interest in understanding how lifestyle choices and social factors affect life expectancy, healthspan, and the onset of chronic age-related diseases, including cancer. Although alcohol is a known carcinogen that accounts for roughly one-third of primary liver cancer cases worldwide, it is not yet known if chronic alcohol consumption by an individual’s parents heritably influences their predisposition to developing liver cancer. Here, we employed our established multiplex mouse model to compare sensitivities of the male offspring of maternal, paternal, and dual-parental alcohol exposures to the potent hepatocellular carcinoma inducer, Diethylnitrosamine (DEN), and determine their predisposition for tumor formation and growth. Our experiments reveal that chronic parental alcohol consumption programs a pro-tumor environment in the liver. This increased cancer susceptibility correlates with increased steatosis, hepatic fibrosis, inflammation, and oxidative stress. Interestingly, some of these changes display accumulative effects and are more pronounced when both parents are exposed to alcohol.
2024-08-05 | GSE273675 | GEO
Project description:Accumulating evidence suggests that lifestyle-related factors may influence radiation responses and the resulting cancer risks through epigenetic mechanisms, such as miRNA regulations. Chronic alcohol consumption is a major risk factor for various pathologies, including alcoholic liver disease. We have recently shown that consumption of Japanese sake promotes glutathione metabolism and anti-oxidative activities in the liver of irradiated C57BL/6 mice. Here we show that chronic alcohol consumption resulted in elevated ciculating levels of the inflammatory cytokine TNF-α and that it triggered specific miRNA regulations (such as the upregulation of the radio-resistant miR-210) that are susceptible to influence the resulting radiation effects in the mouse liver. Japanese sake was administrated to C3H mice irradiated with 3 Gy X-rays. miRNA expression was measured in the livers of 3 mice for each experimental group.
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