Transcriptomic profiling of HepaRG cells with or without fat-loading
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ABSTRACT:
PROVIDER: PRJNA767858 | ENA |
REPOSITORIES: ENA
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Project description:We report whole genome gene expression in HepaRG cells, a human hepatocellular carcinoma cell line, that were either treated with palmitic and oleic acid or solvent only. These data capture transcriptional events related to the response of human hepatocyte-like cells to fat-loading.
2024-01-01 | GSE185169 | GEO
Project description:The present study was aimed to mimic steatosis in in-vitro HepaRG model and test the effect of lipid loading on drug metabolizing enzymes and transporters (DMET) in steatosis. HepaRG cells, differentiated in-house were exposed to mixture of saturated and unsaturated fatty acids, 0.5 mM palmitate and oleate (1:2) conjugated to BSA (0.02%) for 72h. Following the incubation, the model system was characterized using ORO staining for neutral lipids, tested for toxicity with WST-1 assay and triglyceride (TAG) accumulation was measured using TAG calorimetric assay. Increased lipid accumulation and 6-fold increase in TAG was observed (P < 0.05, n=4). The whole transcriptome was analyzed using RNA sequencing. Differentially expressed transcripts were identified upon FA treatment versus (vs.) control in HepaRG cell line (393 total transcripts, 89 up- and 304 downregulated). Lipid loading, led to significant down-regulation in gene expression levels of various DMET, nuclear receptors and transcription factors such as CYP3A4, 1A2, 2B6, 2C8, 2C9 and 2C19, along with this UGT1A9, UGT1A6, ABCB1, NR1I2 and HNF4α (P < 0.05, n=3). The accumulation of saturated and polyunsaturated fatty acids may selectively inhibit certain DME pathways.
2020-12-31 | GSE122151 | GEO
Project description:Comparison of expression profiles detected inundifferemtitated HepaRG cells exposed to DMSO, TCDD for 24h. The aryl hydrocarbon receptor (AhR) activation has been shown to stimulate proliferation, promote apoptosis or alter differentiation of adult rat liver progenitors. We investigated the impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated AhR activation on a human model of bipotent liver progenitors, undifferentiated HepaRG cells. We used both intact undifferentiated HepaRG cells, and HepaRG cells with silenced Hippo pathway effectors, YAP1 and TAZ, which play key role(s) in tissue specific progenitor cell self-renewal and expansion, including liver, cardiac or respiratory progenitors.
2019-09-01 | GSE122518 | GEO
Project description:We studied the effect of propagule on hepatic transcriptome in mice loaded high-fat for four weeks. Improved genes, which were restored the effects of high-fat loading by simultaneous ingestion with propagule, were picked up using hepatic transcriptome analysis. They mainly belonged to immune system and fat metabolism. High-fat loading induced hepatic inflammation, but simultaneous ingestion with propagule repressed it. As for lipid metabolism, propagule was repressed a rise of cholesterol biosynthesis and catabolism by high-fat loading. As for carbohydrate metabolism, propagule was decreased glycolysis, glycogen synthesis and increased gluconeogenesis. Moreover, amino acids were converted into pyruvate, and then they would be used for gluconeogenesis. In conclusion, propagule will be acted to delay the occurrence of hepatic disease by the suppression of carbohydrate and fat metabolism disorder in high-fat loaded mice.
2022-03-01 | GSE127676 | GEO
Project description:The aim of the study was to characterize at a molecular level (changes in mRNA level) the effects of WNT3A on the human HepaRG hepatocellular carcinoma cell line. This was adressed by culturing HepaRG cells in presence or absence of Wnt3a.
2017-02-11 | GSE68633 | GEO
Project description:To identify the molecular mechanisms and environmental inducers contributing to reprogramming of hepatocytes into progenitors in HCC context, we used the HepaRG cell line as model.
2013-12-05 | GSE52989 | GEO
Project description:The canonical mode of action (MOA) of microcystins (MC) is the inhibition of protein phosphatases, but complete characterization of toxicity pathways is lacking. The existence of over 200 MC congeners complicates risk estimates worldwide. This work employed RNA-seq to provide an unbiased and comprehensive characterization of cellular targets and impacted cellular processes of hepatocytes exposed to either MC-LR or MC-RR congeners. The human hepatocyte cell line, HepaRG, was treated with three concentrations of MC-LR or -RR for 2 h. Significant reduction in cell survival was observed in LR1000 and LR100 treatments whereas no acute toxicity was observed in any MR-RR treatment. RNA-seq was performed on all treatments of MC-LR and -RR. Differentially expressed genes and pathways associated with oxidative and endoplasmic reticulum (ER) stress, and the unfolded protein response (UPR) were highly enriched by both congeners as were inflammatory pathways. Genes associated with both apoptotic and inflammatory pathways were enriched in LR1000. We present a model of MC toxicity that immediately causes oxidative stress and leads to ER stress and the activation of the UPR. Differential activation of the three arms of the UPR and the kinetics of JNK activation ultimately determine whether cell survival or apoptosis is favored. Extracellular exosomes were enrichment of by both congeners, suggesting a previously unidentified mechanism for MC-dependent extracellular signaling. The complement system was enriched only in MC-RR treatments, suggesting congener-specific differences in cellular effects. This study provided an unbiased snapshot of the early systemic hepatocyte response to MC-LR and MC-RR congeners and may explain differences in toxicity among MC congeners.
| S-EPMC7670210 | biostudies-literature
Project description:Rapidly increasing number of man-made chemicals urges the development of reliable time- and cost-effective approaches for the carcinogen detection and identification. Considering this, the utility of high throughput microarray gene expression profiling for the identification of genotoxic and non-genotoxic carcinogens in vitro was investigated. Human terminally differentiated hepatic HepaRG cells were treated with model liver carcinogens, genotoxic carcinogen aflatoxin B1 (AFB1) and non-genotoxic carcinogen methapyrilene, at IC10 and IC25 concentrations for 72 hours, and transcriptomic profiles were determined. Treatment of HepaRG cells with IC10 and IC25 concentrations of AFB1 resulted in altered expression of 538 and 3033 genes (p-value ≤0.01 and fold change ≥2.0), respectively, and treatment of HepaRG cells with methapyrilene at the IC10 and IC25 concentrations altered the expression of 1255 and 1861 genes, respectively. Pathway analysis of transcriptomic signatures in HepaRG cells treated with minimally cytotoxic IC10 concentrations of AFB1 and methapyrilene demonstrated a strong enrichment in genes involved in key carcinogen-associated pathways, including receptor-mediated effects, detoxification response, cell death and apoptosis, cell proliferation and survival, oxidative stress and inflammation. Importantly, DNA damage and repair, cell cycle progression, and cell cycle checkpoint control pathways were uniquely activated in AFB1-treated HepaRG cells, whereas receptor-mediated signaling detoxification response pathway was predominantly altered in methapyrilene-treated HepaRG cells. In summary, high throughput microarray gene expression approach identifies specific carcinogen-exposure-associated transcriptomic responses and identifies affected molecular pathways, and categorize pathways associated with carcinogen exposure in a short-term in vitro test.
2016-09-17 | GSE87028 | GEO
Project description:Gene expression profile analysis allowed to identify a panel of genes characteristic of HepaRG differentiation and DMSO effect on the differentiation process.
2022-09-06 | GSE112123 | GEO
Project description:To identify the molecular mechanisms and environmental inducers contributing to reprogramming of hepatocytes into progenitors in HCC context, we used the HepaRG cell line as model. We performed transcriptomic analysis at various time-points during this process; 0h, 1h, 4h, 8h, 12h, 16h, 24h and 48h.
2013-12-05 | E-GEOD-52989 | biostudies-arrayexpress