GEO DataSets

(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:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL18573 GPL19057

30 Samples

Download data: TXT

(Submitter supplied) 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:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

8 Samples

Download data: TXT

(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

(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:

GPL17021 GPL24014

74 Samples

Download data: TXT

(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

(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

(Submitter supplied) Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model.

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4883

Platform:

GPL1261

12 Samples

Download data: CEL

Analysis of livers of animals fed a methionine- and choline- deficient, high fat diet (MCD+HF) containing metformin. MCD+HF models non-alcoholic steatohepatitis (NASH). Results provide insight into the feasibility of using metformin, an anti-diabetic drug, to treat NASH without underlying diabetes.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 protocol sets

Platform:

GPL1261

Series:

GSE35961

12 Samples

Download data: CEL

(Submitter supplied) Interleukin (IL) 11 is upregulated in a number of fibro-inflammatory diseases and cancer, where it binds the cognate IL11 receptor alpha subunit (IL11RA) to form a hexameric IL11:IL11RA:gp130 signalling complex. Primary cells such as hepatic stellate cells, fibroblasts, and hepatocytes are ideal experimental systems to study IL11 signalling in vitro. In contrast to immortalized cell lines, primary cells better capture physiologically relevant cellular physiology and pathobiology. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

16 Samples

Download data: TXT

(Submitter supplied) Here, we developed a mouse model with long-term chronic (8-12 week) plus single/multiple binge ethanol feeding, which mimicks the drinking patterns of AH patients, who often have a history of chronic drinking plus recent excessive drinking. This model produces severe macrosteatosis, significant inflammation, and mild fibrosis. Moreover, we conducted translational studies by comparing transcriptome data from this clinically relevant in vivo model and human AH biopsy samples, and identified many similar disregulated genes in this animal model and AH samples. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

24 Samples

Download data: TXT

(Submitter supplied) Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease where invasive pulmonary myofibroblasts secrete collagen and destroy lung integrity. Here we show that IL-11 is upregulated in the lung of IPF patients, associated with disease severity and is secreted from IPF fibroblasts. In vitro, IL-11 stimulates lung fibroblasts to become invasive, ACTA2+ve, collagen secreting myofibroblasts, in an ERK-dependent fashion. more...

Organism:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL19057 GPL18573

39 Samples

Download data: TXT

(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

(Submitter supplied) In this study we sought to determine if the knockout of hepatocyte PPARgamma expression alter transcriptomics of the livers of mice with diet-induced NASH, and if there was a hepatocyte-specific PPARgamma dependent regulation of gene expression in TZD treated mice. Specifically, adult PPARg floxed male mice were fed a high fat, cholesterol and fructose (HFCF) diet for 24 weeks. After this period of time, half of the mice were injected with AAV8-TBG-Cre to knockout PPARgamma in hepatocytes (KO mice). more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

24 Samples

Download data: XLS

(Submitter supplied) In this study we sought to determine how hepatocyte-specific PPARgamma expression regulates hepatic gene expression in normal (healthy) mice fed a LFCF diet, or mice that were fed a HFCF diet for 24 weeks to induce non-alcoholic steatohepatitis (NASH). Specifically, we used chow-fed adult (10 week-old) PPARgamma floxed male mice and injected them with AAV8-TBG-Cre to knockout PPARgamma in hepatocytes (KO). more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

19 Samples

Download data: XLS

(Submitter supplied) The kidney has large regenerative capacity that is impeded when injured renal tubular epithelial cells (TECs) undergo SNAI1-driven partial epithelial mesenchymal transition (pEMT). Here we investigate the role of IL11 in TEC pEMT and kidney repair. Wild-type mice with acute kidney injury (AKI) upregulate IL11 in TECs triggering an ERK/P90RSK/GSK3β axis of SNAI1 expression leading to impaired renal function, which is abrogated in Il11 null mice. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

16 Samples

Download data: TXT

(Submitter supplied) Adult PPARg floxed male and female mice were fed a high fat diet (HFD) for 16 weeks to induce obesity. Half of these mice were then injected with AAV8-TBG-Cre to knockout PPARg in hepatocytes. The remaining half were injected with AAV8-TBG-Null to generate control mice. After two weeks, mice fed the HFD were either maintained on this diet or switched to a high fat, high cholestrol, high fructose (HFCF) diet for an additional 16 weeks. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

48 Samples

Download data: TXT

(Submitter supplied) In murine NAFL/NASH models, high-fat high-calorie fructose (HFHC) diet fed for 16 weeks induces hepatic steatosis, inflammatory cells infilatration and early stage fibrosis. In addition, HFHC diet 16 weeks but not 8 weeks is accompanied with weight gain and insulin resistance. The aim of this study is to determine the gene expression changes in mouse liver by HFHC diet for 8weeks.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

6 Samples

Download data: TXT

(Submitter supplied) Abnormalities in hepatic lipid metabolism are believed to play a critical role in the etiology of nonalcoholic steatohepatitis (NASH). Monoacylglycerol acyltransferase (MGAT) enzymes convert monoacylglycerol to diacylglycerol, which is the penultimate step in one pathway for triacylglycerol (TAG) synthesis. Hepatic expression of Mogat1, which encodes an MGAT enzyme, is increased in the livers of mice with hepatic steatosis and knocking down Mogat1 improves insulin sensitivity, but whether increased MGAT activity plays a role in the etiology of NASH is unclear. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5425

Platform:

GPL6887

8 Samples

Download data: TXT

Analysis of liver from diet-induced obese males depleted for monoacylglycerol acyltransferase 1 (Mogat1) via intraperitoneal injections of antisense oligonucleotide directed against Mogat1. Results provide insight into the role of Mogat1 in the development of nonalcoholic steatohepatitis (NASH).

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL6887

Series:

GSE60349

8 Samples

Download data

(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