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Next-generation sequencing (NGS) facilitates quantitative analysis of differentially expressed genes in ethanol-fed murine livers after ethanol binge

ABSTRACT: Next-generation sequencing (NGS) facilitates quantitative analysis of differentially expressed genes in ethanol-fed murine livers after ethanol binge

PROVIDER: PRJNA804242 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17923063.fastq.gz	Fastqsanger.gz
	SRR17923064.fastq.gz	Fastqsanger.gz
	SRR17923065.fastq.gz	Fastqsanger.gz
	SRR17923066.fastq.gz	Fastqsanger.gz

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Next-generation sequencing (NGS) facilitates quantitative analysis of differentially expressed genes in ethanol-fed murine livers after ethanol binge

Project description:Purpose: The goals of this study are to use NGS-derived liver transcriptome profiling (RNA-seq) and identify differentially expressed genes in damaged livers that were exposed to 5% ethanol-containing liquid diet and ethanol binge. Methods: Liver mRNA profiles were generated from chronic ethanol feeding plus a single binge by deep sequencing, in duplicate, using Illumina Hiseq2500. qRT–PCR validation was performed using SYBR Green assay. Results: Chronic ethanol feeding plus a single binge treatment was associated with 422 downregulated genes and 384 upregulated genes, whereas Yap1 null livers had 351 downregulated genes and 287 upregulated genes after ethanol/CCl4 induced liver damage. Conclusions: This study provides detailed analysis of liver transcriptomes during hepatocyte damage caused by chronic ethanol feeding plus a single binge treatment, with biologic replicates, generated by RNA-seq technology.

2022-02-10 | GSE196314 | GEO

A novel model of binge ethanol exposure reveals enhanced neurodegeneration with advanced age

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Adolescent binge ethanol impacts H3K36me3 regulation of synaptic genes [ChIP-Seq]

Project description:Adolescence is marked in part by the ongoing development of the prefrontal cortex (PFC). Binge ethanol use during this critical stage in neurodevelopment induces significant structural changes to the PFC, as well as cognitive and behavioral deficits that can last into adulthood. Previous studies showed that adolescent binge ethanol causes lasting deficits in working memory, decreases in the expression of chromatin remodeling genes responsible for the methylation of histone 3 lysine 36 (H3K36), and global decreases in H3K36 in the PFC. H3K36me3 is present within the coding region of actively-transcribed genes, and safeguards against aberrant, cryptic transcription by RNA Polymerase II. We hypothesize that altered methylation of H3K36 could play a role in adolescent binge ethanol-induced memory deficits. To investigate this at the molecular level, ethanol (4g/kg, i.g.) or water was administered intermittently to adolescent mice. RNA- and ChIP-sequencing were then performed within the same tissue to determine gene expression changes and identify genes and loci where H3K36me3 was disrupted by ethanol. We further assessed ethanol-induced changes at the transcription level with differential exon-use and cryptic transcription analysis – a hallmark of decreased H3K36me3. Here, we found ethanol-induced changes to the gene expression and H3K36me3-regulation of synaptic-related genes in all our analyses. Notably, H3K36me3 was differentially trimethylated between ethanol and control conditions at synaptic-related genes, and Snap25 and Cplx1 showed evidence of cryptic transcription in males and females treated with ethanol during adolescence. Our results provide preliminary evidence that ethanol-induced changes to H3K36me3 during adolescent neurodevelopment may be linked to synaptic dysregulation at the transcriptional level, which may explain the reported ethanol-induced changes to PFC synaptic function.

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Adolescent binge ethanol impacts H3K36me3 regulation of synaptic genes [RNA-Seq]

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Project description:We altered the NIAAA (Gao Binge Model) of 8 week chronic plus binge ethanol (E8G1) to have 3 total ethanol gavages (5 g/kg; 1 every 24h) of ethanol after 8 weeks of chronic ethanol feeding (E8G3) to determine how the liver responds to chronic plus consecutive binge ethanol. Surprisingly, E8G3 treatment induced lower levels of liver injury, steatosis, inflammation, and fibrosis as compared to mice after E8G1 treatment. Microarray analyses were performed, identifying several pathways that may contribute to the observed liver adaptation to binge ethanol. In addition, cytochrome P450 2B10 (Cyp2b10) was a top upregulated gene in the E8G1 group and further upregulated in the E8G3 group, but only moderately induced after chronic ethanol consumption, which was confirmed by RT-qPCR and western blot analyses. Genetic disruption of the Cyp2b10 gene worsened liver injury in E8G1 and E8G3 mice with higher blood ethanol levels compared to wild-type control mice, while in vitro experimentation revealed that CYP2b10 did not directly promote ethanol metabolism. Metabolomic analyses revealed significant differences in hepatic metabolites from E8G1-treated Cyp2b10 KO and WT mice, and these metabolic alterations may contribute to the reduced liver injury in Cyp2b10 KO mice.

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RNA-Seq of femoral shaft RNA from Catalase knockout (KO) and wild-type (WT) male mice at 12 weeks of age given binge ethanol or control PBS for four consecutive days.

Project description:The objective was to determine how binge ethanol and knockout of the catalase gene affect the transcriptome of the femoral shaft in mice.

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Project description:Adolescent binge ethanol impacts H3K36me3 regulation of synaptic genes [RNA-Seq]

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Project description:Adolescent binge ethanol impacts H3K36me3 regulation of synaptic genes [ChIP-Seq]

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