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Hepatic transcriptome profiling of liver-specific Xbp1 knockout mice fed a high fat diet

ABSTRACT: Xbp1 is an important regulator of unfolded protein response and lipid metabolism. Its dyregulation has been associcated in human NASH. Feeding a high fat diet with fructose/sucrose to mice causes progressive, fibrosing steatohepatitis. This study is to use RNA-Seq to identify differentially expressed genes in hepatic Xbp1 deficient mice livers fed with a high fat diet compared to controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE64824 | GEO | 2016/01/07

SECONDARY ACCESSION(S): PRJNA271953

REPOSITORIES: GEO

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Hepatic transcriptome profiling of liver-specific Xbp1 knockout mice fed a high fat diet

Project description:Xbp1 is an important regulator of unfolded protein response and lipid metabolism. Its dyregulation has been associcated in human NASH. Feeding a high fat diet with fructose/sucrose to mice causes progressive, fibrosing steatohepatitis. This study is to use RNA-Seq to identify differentially expressed genes in hepatic Xbp1 deficient mice livers fed with a high fat diet compared to controls. Hepatic Xbp1 deficient mice or flox controls were fed either regular chow or a high fat diet (n=4). Samples from each cohort were pooled into two replicates.

2016-01-07 | E-GEOD-64824 | biostudies-arrayexpress

Gene expression profiles of livers and liver tumors from mice fed high-fat diet and high fructose-glucose solution for 52 weeks

Project description:The lack of a preclinical model of nonalcoholic steatohepatitis (NASH) and hepatocellular cancer (HCC) that recapitulates human disease is a major barrier to therapeutic development. We report a high fat-high sugar diet-induced NASH and HCC in a stable isogenic 129S1/SvImJ crossed with C57Bl/6J mice. Following diet initiation, there was sequential development of steatosis (4-8 weeks), steatohepatitis with ballooning and Mallory-Denk bodies (12-16 weeks), progressive fibrosis (16 week onwards) and spontaneous HCC (32-52 weeks). The mice developed obesity, insulin resistance and dyslipidemia. There was concordance with the human NASH transcriptome (FDR 0.001) with activation of lipogenic, inflammatory and apoptotic pathways relevant in humans. The HCC gene signature resembled S1 and S2 human HCC subclass (FDR 0.01 for both). This simple model of NASH and HCC that resembles human disease in terms of its triggers, physiological and biochemical parameters, histology, transcriptomic profile, and outcomes can facilitate preclinical development for these conditions. 129S1/SvImJ;C57Bl/6J (129/B6) mice were fed with high-fat diet (Western Diet) and high fructose-glucose solution (Sugar Water) (WD SW) or chow diet (CD) for 52 weeks, and total RNA samples were isolated from liver and tumor tissues for genome-wide expression profiling.

2016-07-25 | E-GEOD-67679 | biostudies-arrayexpress

Gene expression profiles of livers from mice fed high-fat diet and high fructose-glucose solution for 8 weeks

Project description:The lack of a preclinical model of nonalcoholic steatohepatitis (NASH) and hepatocellular cancer (HCC) that recapitulates human disease is a major barrier to therapeutic development. We report a high fat-high sugar diet-induced NASH and HCC in a stable isogenic 129S1/SvImJ crossed with C57Bl/6J mice. Following diet initiation, there was sequential development of steatosis (4-8 weeks), steatohepatitis with ballooning and Mallory-Denk bodies (12-16 weeks), progressive fibrosis (16 week onwards) and spontaneous HCC (32-52 weeks). The mice developed obesity, insulin resistance and dyslipidemia. There was concordance with the human NASH transcriptome (FDR 0.001) with activation of lipogenic, inflammatory and apoptotic pathways relevant in humans. The HCC gene signature resembled S1 and S2 human HCC subclass (FDR 0.01 for both). This simple model of NASH and HCC that resembles human disease in terms of its triggers, physiological and biochemical parameters, histology, transcriptomic profile, and outcomes can facilitate preclinical development for these conditions. 129S1/SvImJ;C57Bl/6J (129/B6) mice were fed with high-fat diet (Western Diet) and high fructose-glucose solution (Sugar Water) (WD SW) or chow diet (CD) for 8 weeks, and total RNA samples were isolated from liver tissues for genome-wide expression profiling.

2016-07-25 | E-GEOD-67678 | biostudies-arrayexpress

Administration of glutaredoxin-1 attenuates liver fibrosis caused by aging and non-alcoholic steatohepatitis

Project description:Glutaredoxin-1 (Glrx) controls redox signaling and has an anti-apoptotic function. We evaluated the role of Glrx on hepatic cell damage and fibrosis induced by a high-fat diet. We fed mice a high-fat high-fructose diet to induce non-alcoholic steatohepatitis (NASH) and injected AAV-Glrx to express hepatocyte-specific Glrx in diet-induced NASH mice. AAV-Glrx suppressed fibrosis and improved liver function in the NASH liver. We used microarrays to profile gene expression in the NASH liver and find pathways that AAV-Glrx mediated to attenuate fibrosis and NASH progression.

2022-06-01 | GSE198961 | GEO

Transcriptomic analysis of liver mRNA from liver-specific Pck1-knockout mice fed with chow diet or NASH diet

Project description:To investigate the role of hepatic Pck1 in diet-induced nonalcoholic steatohepatitis (NASH), liver-specific Pck1-knockout mice were developed with Alb-Cre. Wild-type (WT) and Pck1-cKO mice were fed a Chow diet (Research Diets, D12450J: 10% Kcal fat, with tap water) or NASH-inducing diet (Research Diets, D12492: 60% Kcal fat, with drinking water containig 23.1 g/L fructose and 18.9 g/L glucose) for 24 weeks. RNA was extracted from the livers of mice from all treatment groups and used for RNA seqencing. RNA-seq data demonstrated that gluconeogenic enzyme PCK1 deficiency played an important role in the development of NASH.

2023-02-07 | GSE162211 | GEO

Platelet-derived thrombospondin 1 promotes immune cell liver infiltration and exacerbates diet-induced steatohepatitis.

Project description:Background and Aims: Recent studies have implicated platelets, particularly α-granules, in the development of steatohepatitis (NASH). However, the specific mechanisms involved have yet to be determined. Notably, thrombospondin 1 (TSP1) is a major component of the platelet α-granules released during platelet activation. The role of platelet-derived TSP1 in NASH remains unknown and was investigated in this study. Approach and Results: Platelet-specific TSP1 knockout mice (TSP1Δpf4) and their wild type littermates (TSP1F/F) were used. NASH was induced by feeding the mice a diet enriched in fat, sucrose, fructose, and cholesterol (AMLN diet). A human liver NASH organoid model was also employed. Although TSP1 deletion in platelets did not affect diet-induced steatosis, TSP1Δpf4 mice exhibited attenuated NASH and liver fibrosis, accompanied by improvements in plasma glucose and lipid homeostasis. Moreover, intrahepatic platelet accumulation, activation and chemokine production were reduced in TSP1Δpf4 mice, which was correlated with decreased immune cell infiltration into the liver. Consequently, this leads to diminished pro-inflammatory signaling in the liver and mitigated the progression of NAFLD. Moreover, in vitro data revealed that co-culturing TSP1-deficient platelets in a human liver NASH organoid model attenuated hepatic stellate cell activation and NASH progression. Additionally, TSP1 deficient platelets play a role in regulating brown fat endocrine function, specifically affecting Nrg4 production. Crosstalk between brown fat and the liver may also influence NAFLD progression. Conclusions: These data suggest that platelet α-granule-derived TSP1 is a significant contributor to diet-induced NASH and fibrosis, and may serve as a new therapeutic target for this severe liver disease.

2024-03-13 | GSE250004 | GEO

Small RNA profiling of Simple steatosis and Non-alcoholic steatohepatitis in the liver of mice [miRNA-seq]

Project description:In our study, C57BL/6 male mice were fed a normal chow diet or high-fat diet additionally containing high-fructose and high-cholesterol (HFHC diet) for 12 weeks and 28 weeks to construct simple steatosis (NAFL) and Non-alcoholic steatohepatitis (NASH) models respectively. Through miRNA sequencing, 420 miRNAs were detected. A total of 148 miRNAs (14 up-regulated and 34 down-regulated) and 146 miRNAs (74 up-regulated and 72 down-regulated) were differentially expressed in livers of NAFL and NASH mice, respectively. A total of 36 miRNAs (8 up-regulated; 28 down-regulated) were dysregulated in both NASH and NAFL mice, while 110 miRNAs (66 up-regulated; 44 down-regulated) were altered specifically in NASH mice.

2022-03-26 | GSE199246 | GEO

Long non-coding RNA profiling of Simple steatosis and Non-alcoholic steatohepatitis in the liver of mice

Project description:In our study, C57BL/6 male mice were fed a normal chow diet or high-fat diet additionally containing high-fructose and high-cholesterol (HFHC diet) for 12 weeks and 28 weeks to construct simple steatosis (NAFL) and Non-alcoholic steatohepatitis (NASH) models respectively. Through lncRNA sequencing, a total of 1131 lncRNAs (798 up-regulated and 333 down-regulated) and 5161 lncRNAs (3168 up-regulated and 1993 down-regulated) were differentially expressed in livers of NAFL and NASH mice respectively. A total of 614 lncRNAs (455 up-regulated and 159 down-regulated) were dysregulated in both NASH and NAFL mice, while 4547 lncRNAs (2713 up-regulated; 1834 down-regulated) were altered specifically in NASH mice.

2022-03-27 | GSE199306 | GEO

Dietary cholesterol promotes fatty liver-associated liver cancer by inducing aberrant genomic expression and mutations

Project description:We investigated the effects of cholesterol on nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) in diethylnitrosamine-injected mice fed high-fat high-cholesterol (HFHC) diet versus high-fat (HF) alone. mRNA microarray analysis was applied for expressional aberrations.

2018-09-27 | E-MTAB-6002 | biostudies-arrayexpress

Genome-wide open chromatin analysis of liver sinusoidal endothelial cells in the pathogenesis of NASH

Project description:We isolated liver sinusoidal endothelial cells (LSEC) from mice fed control chow (Chow) or the nonalcoholic steatohepatitis (NASH)-inducing high fat, fructose and cholesterol (FFC) diet, and subjected the cells to Omni-ATAC-seq. Out of the top 500 differentially abundant open chromatin regions between the two groups, 498 were more robust in FFC-fed mice compared with Chow-fed mice, suggesting a genome-wide active epigenetic regulation in LSEC during NASH development. Furthermore, in combination with RNA-seq, we demonstrated a robust transcriptional upregulation of the adhesion molecule VCAM-1 in LSEC in NASH pathogenesis.

2021-02-01 | GSE164008 | GEO

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