Project description:Full title: Mercury-Induced Hepatotoxicity in Zebrafish: In Vivo Mechanistic Insights from Transcriptome Analysis, Phenotype Anchoring and Targeted Gene Expression Validation In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 200 µg/L of mercuric chloride for 8-96 h, to identify global transcriptional programs and biological pathways involved in mercury-induced adaptive responses under in vivo environment. We analyzed 12 arrays for mercuric chloride treated zebrafish liver and 12 arrays for control liver.
Project description:Abstract: Paired-end sequence data has been generated using polyA selected RNA from a range of zebrafish tissues using the Illumina Genome Analyzer. Study description: Zebrafish total RNA was extracted from adult tissue, then polyA selected. After fragmentation and reverse transcription Illumina sequencing libraries were prepared. Paired-end sequence runs were performed with 76 base reads on the Illumina Genome Analyzer. ArrayExpress Release Date: 2011-01-28 Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30608 | GEO
Project description:Transcriptomic profiles of zebrafish liver exposed to phenanthrene
Project description:Full title: Mercury-Induced Hepatotoxicity in Zebrafish: In Vivo Mechanistic Insights from Transcriptome Analysis, Phenotype Anchoring and Targeted Gene Expression Validation In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 200 µg/L of mercuric chloride for 8-96 h, to identify global transcriptional programs and biological pathways involved in mercury-induced adaptive responses under in vivo environment.
Project description:Condition specific zebrafish metabolic models generated using the COBRA MetaboTools framework. The Wang et al., (2021) zebrafish genome-scale metabolic model (GEM) was constrained with experimental data from 5 days post fertilized (dpf) zebrafish to generate a 'base-model'.
In turn this 5 dpf zebrafish base-model was constrained with experimental (transcriptomics and metabolomics) data from 5 dpf zebrafish exposed to the environmental pollutant perfluorooctane sulfonate (PFOS), at three levels - Low (0.06 uM), Medium (0.6 uM), and High (2 uM) PFOS.
The MetaboTools framework was used to construct three condition-sepcific models: Low, Medium, and High PFOS.
Key simulation predictions of effects on the carnitine shuttle and lipid metabolism were confirmed in wild-caught fish and dolphins (stranded animals) sampled from the northern Gulf of Mexico - published in Nolen et al., (2024) https://doi.org/10.1016/j.cbpc.2023.109817
Project description:To investigate the transcriptional changes following acute liver injury, we exposed WT and Nrf2KO zebrafish larvae to APAP for 12 and 24 hours. We then dissected out zebrafish larval livers and pooled 20 livers per sample for RNA-seq.
Project description:Exposure to bisphenol A (BPA), an endocrine disruptor (ED), has raised concerns for both human and ecosystem health. Epigenetic factors, including microRNAs, are key regulators of gene expression during cancer. The effect of BPA exposure on the zebrafish epigenome remains poorly characterized. Zebrafish represents an excellent model to study cancer as the organism develops disease that resembles human cancer. Using zebrafish as systems toxicology model, we hypothesized that chronic BPA-exposure impacts the miRNome in adult zebrafish and establishes an epigenome more susceptible to cancer development. After a 21 day exposure to 100 nM BPA, RNA from the liver was extracted to perform high throughput mRNA and miRNA sequencing. Differential expression (DE) analyses comparing BPA-exposed to control specimens were performed using established bioinformatics pipelines. In the BPA-exposed liver, 6,188 mRNAs and 15 miRNAs were differently expressed (q ≤ 0.1). By analyzing human orthologs of the DE zebrafish genes signatures associated with non-alcoholic fatty liver disease (NAFLD), oxidative phosphorylation, mitochondrial dysfunction and cell cycle were uncovered. Chronic exposure to BPA has a significant impact on the liver miRNome in adult zebrafish and has the potential to cause adverse outcomes including cancer.
Project description:Experiment exposed adult male zebrafish to 10ng/L 17-alpha ethinylestradiol for three weeks. Gene expression profiling of liver and telencephalon following exposure. Keywords: estrogenic exposure
Project description:Exposure to bisphenol A (BPA), an endocrine disruptor (ED), has raised concerns for both human and ecosystem health. Epigenetic factors, including microRNAs, are key regulators of gene expression during cancer. The effect of BPA exposure on the zebrafish epigenome remains poorly characterized. Zebrafish represents an excellent model to study cancer as the organism develops disease that resembles human cancer. Using zebrafish as systems toxicology model, we hypothesized that chronic BPA-exposure impacts the miRNome in adult zebrafish and establishes an epigenome more susceptible to cancer development. After a 3 week exposure to 100 nM BPA, RNA from the liver was extracted to perform high throughput mRNA and miRNA sequencing. Differential expression (DE) analyses comparing BPA-exposed to control specimens were performed using established bioinformatics pipelines. In the BPA-exposed liver, 6,188 mRNAs and 15 miRNAs were differently expressed (q ≤ 0.1). By analyzing human orthologs of the DE zebrafish genes, signatures associated with non-alcoholic fatty liver disease (NAFLD), oxidative phosphorylation, mitochondrial dysfunction and cell cycle were uncovered. Chronic exposure to BPA has a significant impact on the liver miRNome in adult zebrafish and has the potential to cause adverse outcomes including cancer.