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Links from GEO DataSets

Items: 19

1.

Intestinal B cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcR signalling

(Submitter supplied) Non-alcoholic steatohepatitis (NASH), which is increasing in incidence due to the obesity epidemic, is a T-cell mediated, auto-aggressive condition that can result in progressive liver disease and hepatocellular carcinoma (HCC). The gut-liver axis contributes to NASH, yet mechanisms underlying metabolic T-cell activation and NASH-related fibrosis have largely remained elusive. We found that gastrointestinal B-cells are activated and increased in number in mouse/human NASH, allowing metabolic T-cell activation to induce NASH antigen- and microbiota-independently. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: TAR
Series
Accession:
GSE190204
ID:
200190204
2.

Dietary intervention reverses molecular signatures of hepatocellular senescence in the GAN diet-induced obese and biopsy-confirmed mouse model of NASH

(Submitter supplied) We applied RNA sequencing (RNA-seq) to study the effects of dietary intervention on hallmarks of NASH and molecular signatures of hepatocellular senescence in the Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mouse model of NASH. GAN DIO-NASH mice with liver biopsy-confirmed NASH and fibrosis received dietary intervention by switching to chow feeding (chow reversal) for 8, 16, or 24 weeks. Untreated GAN DIO-NASH mice and chow-fed C57BL/6J mice served as controls. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
55 Samples
Download data: TXT
Series
Accession:
GSE246328
ID:
200246328
3.

The synergestic effects of western diet and carbon tetrachloride (CCl4) to develop non-alcoholic steatohepatitis (NASH) and liver tumor in mice

(Submitter supplied) NASH is a combination of hepatic steatosis and severe inflammation, which can lead to fatal liver disease such as cirrhosis and hepatocellular carcinoma. While a variety of models have been descirbed, they have several limitations. Therefore, it is of urgent importance to create animal model that recapitulate the physiology, histology and outcome seen in human with NASH. We created western diet-fed and CCl4-treated mouse model. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE99010
ID:
200099010
4.

MicroRNA-223 ameliorates nonalcoholic steatohepatitis and cancer by targeting multiple inflammatory and oncogenic genes in hepatocytes

(Submitter supplied) Here, we found that microRNA-223 (miR-223) was highly elevated in hepatocytes after high fat diet (HFD) feeding in mice and in human nonalcoholic steatohepatitis (NASH) samples. Genetic deletion of the miR-223 induced a full spectrum of nonalcoholic fatty liver disease (NAFLD) in mice after long-term (up to one year) HFD feeding including NASH-related steatosis, inflammation, fibrosis and HCC. To better explore the mechanisms underlying the abnormalities observed in HFD-fed miR-223KO mice, we examined hepatic gene expression in 3-month-HFD-fed WT and miR-223KO mice by microarray analysis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
8 Samples
Download data: TXT
Series
Accession:
GSE129080
ID:
200129080
5.

Semaglutide reduces tumor burden in the GAN diet-induced obese and biopsy-confirmed mouse model of NASH-HCC with advanced fibrosis

(Submitter supplied) We applied RNA sequencing (RNA-seq) to study the gene expression profile in the liver of GAN DIO-NASH-HCC mice (non-tumorous tissue samples, n=9; tumor samples, n=9) and chow-fed controls (healthy liver samples, n=5)). Comparing tumour tissue of GAN DIO-NASH-HCC mice to healthy chow-fed controls, we find that tumors of GAN DIO-NASH-HCC mice show widespread regulations of genes associated with human HCC. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
23 Samples
Download data: TXT
Series
Accession:
GSE243976
ID:
200243976
6.

A defect in endothelial autophagy occurs in patients with nonalcoholic steatohepatitis and promotes inflammation and fibrosis

(Submitter supplied) Autophagy is a physiological process controlling endothelial homeostasis in vascular beds outside the liver. This study demonstrates that autophagy is defective in liver endothelial cells of patients with NASH and that this defect promotes liver inflammation and fibrosis at early stages of NASH, but also at advanced stages of chronic liver disease. We used transcriptomic analysis to evaluate the global effect of autophagy deficiency in liver sinusoidal endothelial cells' (LSECs) gene expression
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL23038
11 Samples
Download data: CEL
Series
Accession:
GSE138875
ID:
200138875
7.

A preclinical mouse model of nonalcoholic steatohepatitis and hepatocellular cancer that mimics human disease

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
25 Samples
Download data
Series
Accession:
GSE67680
ID:
200067680
8.

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

(Submitter supplied) 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). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
15 Samples
Download data: TXT
Series
Accession:
GSE67679
ID:
200067679
9.

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

(Submitter supplied) 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). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
10 Samples
Download data: TXT
Series
Accession:
GSE67678
ID:
200067678
10.

Gene Expression Analysis of the response to ACC inhibition

(Submitter supplied) BACKGROUND & AIMS: Nonalcoholic steatohepatitis (NASH) is a chronic liver disease characterized by hepatic lipid accumulation, inflammation, and progressive fibrosis. Acetyl-CoA carboxylase (ACC) catalyzes the rate-limiting step of de novo lipogenesis and regulates fatty-acid beta-oxidation in hepatocytes. ACC inhibition reduces hepatic fat content and markers of liver injury in NASH patients; however, the effect of ACC inhibition on liver fibrosis has not been reported. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24014 GPL17021
74 Samples
Download data: TXT
Series
Accession:
GSE148849
ID:
200148849
11.

Transcriptomic analysis of liver mRNA from TSP-1 KO and WT mice fed with normal diet or choline deficient amino acid defined diet (CDAHFD, human NASH model)

(Submitter supplied) Transcriptomic profiles of wild type and TSP1 knockout mice that were fed control (normal) diet or CDAHFD (choline deficient amino acid defiend high fat diet) chow for 12 weeks to model Non-alcoholic Steatohepatitis (NASH) disease in humans.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
20 Samples
Download data: TXT
Series
Accession:
GSE120977
ID:
200120977
12.

IL-11 neutralising therapies for the treatment of nonalcoholic steatohepatitis

(Submitter supplied) Background and aims: Here we investigate the role of IL-11 signalling in the pathogenesis of nonalcoholic steatohepatitis (NASH). Methods: HSCs or hepatocytes were stimulated with IL-11 and effects assessed using cellular and high content imaging, immunoblotting, ELISA and invasion assays. Genetic and pharmacological IL-11 gain- or loss-of-function experiments were performed in vitro and in vivo. IL-11 signaling was studied using ERK inhibitors. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
30 Samples
Download data: TXT
Series
Accession:
GSE128940
ID:
200128940
13.

Shp-deletion induces dissociation of steatosis and inflammation in NASH

(Submitter supplied) Two months-old Shp flox/flox male mice were injected with either AAV8 expressing Cre recombinase driven by the thyroxine-binding globulin (Tbg) promoter (AAV8-Tbg-Cre) or control AAV8 (AAV8-Tbg-null) and fed chow or a diet enriched in high fat, cholesterol, and fructose (Research diet D09100301: 40 kcal% fat, 2% cholesterol, 20 kcal% fructose, hereafter referred to as HFCF diet) for 3 months. Liver RNA was isolated and submitted to RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL15103
12 Samples
Download data: TXT
Series
Accession:
GSE133566
ID:
200133566
14.

Macrophage-derived thrombospondin1 promotes obesity-associated non-alcoholic fatty liver disease

(Submitter supplied) Thrombospondin 1 (TSP1) is a multifunctional matricellular protein. Previously we have shown that TSP1 plays an important role in obesity-associated metabolic complications including inflammation, insulin resistance, cardiovascular and renal disease. However, its contribution to obesity-associated non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH) remains largely unknown and is determined in this study. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
12 Samples
Download data: TXT
Series
Accession:
GSE155973
ID:
200155973
15.

Therapeutic Inhibition of Inflammatory Monocyte Recruitment Reduces Steatohepatitis and Liver Fibrosis

(Submitter supplied) The CCR2/CCR5 inhibitor cenicriviroc blocks infiltration of inflammatory monocytes into the liver, thereby reducing NASH progression and fibrosis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT, XLSX
Series
Accession:
GSE98782
ID:
200098782
16.

The immunoregulatory effects of CD8 T cell-derived perforin on diet-induced nonalcoholic steatohepatitis

(Submitter supplied) Method: To better understand the mechanism of perforin in regulating liver CD8 T cell-mediated inflammation during NASH, we sorted CD8 T cells from the livers of WT or Prf1null mice fed the MCD diet for 4 weeks and performed mRNA sequencing of these hepatic CD8 T cells. Total RNA was isolated from FACS-separated hepatic CD8 T cells. Transcriptome sequencing libraries were generated using NEBNext® Ultra™ RNA Library Prep Kit for Illumina® (NEB, USA) following manufacturer’s recommendations and sequenced on an Illumina Hiseq platform (Illumina, San Diego, CA). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: XLSX
Series
Accession:
GSE121328
ID:
200121328
17.

NCOA5 haploinsufficiency in myeloid cells sufficiently causes non-alcoholic steatohepatitis and hepatocellular carcinoma

(Submitter supplied) Molecular and cellular mechanisms causing the onset and progression of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and HCC remain poorly understood. Here we show that myeloid-cell-specific heterozygous deletion of Ncoa5 (Ncoa5ΔM/+) sufficiently causes the development of NAFLD/NASH and HCC in male mice. The platelet factor 4 (PF4) overexpressed by Ncoa5ΔM/+ intrahepatic macrophages is identified as a potent mediator to trigger lipid accumulation in hepatocytes by inducing expression of genes promoting lipogenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
8 Samples
Download data: CSV, TAR
Series
Accession:
GSE192554
ID:
200192554
18.

Potential utility of L-carnitine for preventing liver tumors derived from metabolic dysfunction-associated steatohepatitis

(Submitter supplied) We examined the potential utility of L-carnitine for alleviating metabolic dysfunction-associated steatohepatitis (MASH) and preventing the development of hepatocellular carcinoma. Short-term L-carnitine administration ameliorated MASH through its anti-inflammatory effects.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
10 Samples
Download data
Series
Accession:
GSE261938
ID:
200261938
19.

Spontaneous cholemia in C57BL/6 mice predisposes to liver cancer in NASH

(Submitter supplied) C57BL/6 mice are the most widely used inbred strain for metabolic and interventional studies. It is commonly known that high-caloric diet feeding induces a heterogeneous phenotype in C57BL/6 mice similar to humans with the majority developing obesity and metabolic dysfunction whilst others remaining lean and metabolically healthy. Nevertheless, the underlying mechanism(s) for this remains unknown. Here, we show that a subset (5-25%) of all C57BL/6 mice develop spontaneous cholemia with elevated total serum bile acids and increased liver damage at early time points upon high-caloric diet feeding. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
7 Samples
Download data: TXT
Series
Accession:
GSE188645
ID:
200188645
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