Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatic microRNA signatures in experimental nonalcoholic steatohepatitis

ABSTRACT: Two-month-old C57BL/6J male mice were placed on chow diet or a diet enriched in high fat, cholesterol, and fructose (Research diet D09100301: 40 kcal% fat, 2% cholesterol, 20 kcal% fructose, HFCF diet) for 1 or 3 months. Liver RNA was isolated and submitted for small RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE135106 | GEO | 2020/03/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA sequencing analysis of hepatic transcriptome profiles in experimental nonalcoholic steatohepatitis

Project description:Two-month-old C57BL/6J male mice were placed on either chow diet or a diet enriched in high fat, cholesterol, and fructose (Research diet D09100301: 40 kcal% fat, 2% cholesterol, 20 kcal% fructose, HFCF diet) for 1 or 3 months. RNA-seq was used to analyze hepatic gene expression from mice on 1-month chow diet, 1-month HFCF diet, 3-month chow diet, and 3-month HFCF.

2019-12-10 | GSE135050 | GEO

Shp-deletion induces dissociation of steatosis and inflammation in NASH

Project description: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.

2019-12-10 | GSE133566 | GEO

Effect of hepatocyte-specific PPARgamma knock out in the regulation of hepatic gene expression in mice fed a low fat diet or and high fat, cholesterol and fructose diet that induces NASH

Project description: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). A subset of PPARgamma floxed mice were injected with AAV8-TBG-Null to generate controls (C). Two weeks after AAV injections, half of the mice in each group were fed a low fat, cholesterol and fructose (LFCF) diet, or a high fat, cholesterol and fructose (HFCF) diet for 24 weeks. Livers were collected at the end of the study to assess hepatic gene expression with RNA-seq (performed by Novogen, Inc.)

2021-01-15 | GSE162249 | GEO

Effect of hepatocyte-specific PPARgamma knock out with and without rosiglitazone treatment in hepatic gene expression of mice with diet-induced NASH

Project description: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). The other half of the mice were injected with AAV8-TBG-Null, and served as controls (C mice). A subset of PPARg floxed mice were fed a low fat, cholesterol and fructose (LFCF) diet, and they were injected with AAV8-TBG-Null to generate LFCF-controls. Two weeks after AAV8 injections, half of the HFCF-fed mice in each group (C and KO) were switched to a HFCF diet containing rosiglitazone maleate (TZD, 50mg/kg of diet) for eight additional weeks. Mice were kept in their respective diets for 8 additional weeks too. At the end of the study, the livers were collected to assess hepatic gene expression with RNA-seq (performed by Novogen, Inc.)

2021-01-15 | GSE162276 | GEO

Transcriptomic Analysis Identifies Dysregulated Aortic Ceramide Metabolism in a Miniature Pig Model of Atherosclerosis

Project description:Dysregulation of lipid metabolism is the pathological basis of the occurrence and development of atherosclerosis.The pig is an ideal animal to study human cardiovascular diseases. However, the specific changes of lipid metabolism in its atherosclerotic plaques, as well as the underlying mechanisms, remain to be elucidated. To investigate the alterations of lipid metabolism related pathways, especially ceramide synthesis related genes, in the abdominal aorta of atherosclerotic pigs induced by high-fat, high-cholesterol, and high-fructose (HFCF) diet, we performed RNA-Seq on abdominal aorta tissue from Wuzhishan pigs fed either normal chow diet or HFCF diet for six months.

2024-01-31 | GSE245530 | GEO

M-NM-2-Cryptoxanthin suppresses inflammatory gene expression in diet-induced nonalcoholic steatohepatitis in mice

Project description:To evaluate the effect of M-NM-2-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% M-NM-2-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, M-NM-2-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although M-NM-2-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. M-NM-2-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by M-NM-2-cryptoxanthin. M-NM-2-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFM-NM-1-inducible genes and the antioxidant enzyme glutathione peroxidase 1 in NASH. Thus, M-NM-2-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH. Eight-week old male C57BL/6J mice were fed for 12 weeks on a CRF-1 standard chow (control), a high-cholesterol and high-fat diet (CL diet; 38.23% CRF-1, 60% cocoa butter, 1.25% cholesterol, 0.5% sodium cholate) or a CL diet containing 0.003% M-NM-2-cryptoxanthin.

2014-05-28 | E-GEOD-51432 | biostudies-arrayexpress

Heterozygous midnolin knockout attenuates severity of nonalcoholic fatty liver disease in mice fed a Western-style diet high in fat, cholesterol, and fructose

Project description:We found that global heterozygous midnolin knockout attenuated the severity of nonalnonalcoholic fatty liver disease (NAFLD) in mice fed a Western-style diet, high in fat, cholesterol, and fructose. This attenuation in disease was associated with significantly reduced levels of large lipid droplets, hepatic free cholesterol, and serum LDL, with significantly differential gene expression involved in cholesterol/lipid metabolism.

2023-05-03 | GSE226810 | GEO

Effect of hepatocyte-specific PPARgamma (PPARg)expression and diet-induced NASH in the liver transcriptome of male and female mice with pre-stablished diet-induced obesity

Project description: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. This study was designed to examine whether the loss of hepatocyte PPARg in mice with established obesity would alter the liver transcriptomics in a PPARg dependent manner when the mice are fed a HFD or a HFCF diet.

2023-01-11 | GSE200352 | GEO

Impact of dietary cholesterol on Macrophages during non-alcoholic steatohepatitis progression

Project description:Inflammation, mediated by liver-resident Kupffer cells (KCs) and recruited infiltrating macrophages (IMs), plays a critical role in NAFLD pathogenesis. Cholesterol induces pro-inflammatory cytokine production by macrophages and has been identified as a key factor involved in progression from simple steatosis to NASH. In this study, using the fructose, palmitate, cholesterol & trans-fat (FPC) diet model which recapitulates human NAFLD, we aimed to determine the impact of cholesterol manipulation on NAFLD progression/regression and macrophage phenotype in vivo.The transcriptomic evaluation of hepatic macrophages from mice fed with FPC diet contained the highest concentration of cholesterol (1.25%) suggest these cells might contribute to liver inflammation, steatohepatitis, and hepatocarcinoma pathways during the progression phase.

2022-08-23 | GSE205776 | GEO

β-Cryptoxanthin suppresses inflammatory gene expression in diet-induced nonalcoholic steatohepatitis in mice

Project description:To evaluate the effect of β-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% β-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, β-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although β-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. β-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by β-cryptoxanthin. β-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFα-inducible genes and the antioxidant enzyme glutathione peroxidase 1 in NASH. Thus, β-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH.

2014-05-28 | GSE51432 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data