Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE199306 | GEO | 2022/03/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Liver Transcriptomes of Simple steatosis in Mice

Project description:In our study, we constructed a Simple steatosis (NAFL) mouse model with a high-fructose and high-cholesterol (HFHC diet) for 12 weeks. Next, we performed RNA Sequencing analysis to reveal molecular features of Simple steatosis. As a result, we obtained hepatic genome-wide mRNA expression in the livers from two groups of mice (NAFL versus Normal).Using FDR < 0.01 and fold change > 2 as the threshold, we identified 176 differentially expressed genes (DEGs) in the livers of NAFL mice relative to the normal control mice, of which 118 up-regulated and 58 down-regulated. The top 5 up-regulated genes in NAFL mice included the genes encoding for Themis, Cfd, Aqp8, Osbpi3 and Scd1.

2022-03-25 | GSE199121 | GEO

Changes of hepatic gene expression in C57BL/6N male mice fed high-fat high-calorie fructose (HFHC) diet for 8 weeks

Project description: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.

2021-12-08 | GSE154426 | GEO

Effects of NAFLD/NASH on hepatic gene expression.

Project description:To characterize gene expression changes in arachidonic acid metabolism pathway genes in the presense of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) mice administered were administered an atherogenic diet for a period of four weeks. Administration of the atherogenic diet resulted in significant enrichment of the arachidonic acid metabolism pathway by gene set enrichment analysis (GSEA). The core enrichment subset of genes was down-regulated in mice administered the atherogenic diet and the majority of the genes that were down-regulated were cytochrome P450s. A total of 4 wild-type mice were administered a standard diet (STD; control group) and 4 wild-type mice were administered a HFHC diet (HFHC).

2014-01-03 | E-GEOD-53381 | biostudies-arrayexpress

Sparcl1 promotes nonalcoholic steatohepatitis progression through upregulation of CCL2

Project description:1. White adipose tissues (WAT) are capable of secreting not only fatty acids but also a class of secretory proteins that modulate the homeostasis of distant organs, including the liver. To identify potential WAT-enriched secretory factors involved in NASH progression, C57BL/6 male mice were fed with a normal chow diet or HFHC diet for two different periods: 12 weeks and 28 weeks. Then, we compared the expression profile of epididymal WAT (eWAT) from mouse models of NAFL and NASH above mentioned by RNA-Sequencing analysis. 2. To investigate the contribution of Sparcl1 in the pathogenesis of NASH, male C57BL/6J mice were fed a HFHC diet for 12 weeks, and then intraperitoneal injected with saline or recombinant Sparcl1 protein (0.2mg/kg) every other day for 3 weeks. To elucidate the molecular basis of Sparcl1-mediated NASH progression, we conducted RNA-Sequencing analysis for differentially expressed genes using the livers of chronic recombinant Sparcl1 protein or saline- treated mice.

2021-06-10 | GSE176681 | 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

Microarray analysis among non-alcoholic fatty liver, non-alcoholic steatohepatitis, and type 2 diabetes mellitus rats

Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes. There are 12 samples in our study which belonged to 4 groups, and each group contains 3 different samples.

2015-01-23 | E-GEOD-65220 | biostudies-arrayexpress

Liver Transcriptomes of Non-alcoholic Steatohepatitis in Mice

Project description:Non-alcoholic steatohepatitis (NASH), has emerged as a major cause of liver failure and hepatocellular carcinoma. Although decades of studies have improved our understanding of its pathophysiology, the molecular mechanisms are still incompletely understood. In the current study, using a diet-induced mouse model of NASH, we performed RNA Sequencing analysis to reveal molecular features of NASH progression. As a result, we obtained hepatic genome-wide mRNA expression in the livers from two groups of mice (NASH versus Normal).Using FDR < 0.01 and fold change > 2 as the threshold, we identified 1745 differentially expressed genes (DEGs) in the livers of NASH mice relative to the normal control mice, of which 1484 up-regulated and 261 down-regulated. The top 5 up-regulated genes included the genes encoding for Trem2, Lcn2, Ephb2, Mmp12 and Sprr1a.Gene ontology (GO) analysis showed that the up-regulated genes in NASH mice were mainly enriched in biological processes such as response to biotic stimulus, regulation of immune system process and myeloid leukocyte activation, while down-regulated genes were related to organonitrogen compound biosynthetic process and organic acid metabolic process.KEGG pathway enrichment results showed that up-regulated genes were mainly enriched in toll like receptor signaling, regulation of actin cytoskeleton, leukocyte transendothelial migration, chemokine signal pathway as well as cytokine and cytokine receptor interaction, while down-regulated gene clusters were mainly enriched in and steroid biosynthetic as well as glycine serine and threonine metabolism.Meanwhile, as expected, genes involved in hepatic lipogenesis (Srebp-1c, Fasn and Scd-1), lipid absorption (CD36), inflammation (Tnfa, IL1b and Ccl2), and fibrosis (Col1a1, Tgfb1 and Mmp13), are up-regulated in NASH mice.Our study may help to uncover NASH molecular basis and provide therapeutic targets for its treatment.

2021-11-20 | GSE189066 | GEO

Microarray analysis of gene expression in the livers of C57BL/6J mice fed a choline- and folate-deficient diet

Project description:Non-alcoholic steatohepatitis (NASH) is becoming one of the leading causes of hepatocellular carcinoma (HCC), replacing viral HBV-, HCV-, and alcohol-related chronic liver diseases as major etiological risk of factors for HCC. The goal of the present study was to investigate transcriptomic alterations in the livers of male C57BL/6J mice fed a choline- and folate-deficient (CFD) diet. Feeding mice a CFD diet for 12 weeks caused NASH-like liver injury exhibiting uniform morphological features of human NASH. High-throughput whole-genome transcriptomic analysis showed that 1750 genes were differentially expressed (344 down-regulated and 1396 up-regulated) in the livers of mice fed a CFD diet as compared to control mice. The functional pathway analysis revealed that these differentially-expressed genes were associated with diverse cellular processes, including cellular growth and differentiation, cell-to-cell signaling and interaction, lipid metabolism, inflammation, fibrosis, molecular transport, and drug metabolism. These findings demonstrate that deregulation of global gene expression is the prominent fundamental feature of NASH in mice induced by a CFD diet.

2017-03-23 | GSE96936 | GEO

MCLR-elicited hepatic fibrosis and carcinogenic gene expression changes persist in rats with diet-induced nonalcoholic steatohepatitis through a 4-week recovery period

Project description:Nonalcoholic steatohepatitis (NASH) causes liver extracellular matrix (ECM) remodeling and is a risk factor for fibrosis and hepatocellular carcinoma (HCC). Microcystin-LR (MCLR) is a hepatotoxin produced by fresh-water cyanobacteria that causes a NASH-like phenotype, liver fibrosis, and is also a risk factor for HCC. The focus of the current study was to investigate and compare hepatic recovery after cessation of MCLR exposure in healthy versus NASH animals. Male Sprague-Dawley rats were fed either a control or a high fat/high cholesterol (HFHC) diet for eight weeks. Animals received either vehicle or 30 µg/kg MCLR (i.p: 2 weeks, alternate days). Animals were euthanized at one of three time points: at the completion of the MCLR exposure period and after 2 and 4 weeks of recovery. Histological staining suggested that after four weeks of recovery the MCLR-exposed HFHC group had less steatosis and more fibrosis compared to the vehicle-exposed HFHC group and MCLR-exposed control group. RNA-Seq analysis revealed dysregulation of ECM genes after MCLR exposure in both control and HFHC groups that persisted only in the HFHC groups during recovery. After 4 weeks of recovery, MCLR hepatotoxicity in pre-existing NASH persistently dysregulated genes related to cellular differentiation and HCC. These data demonstrate impaired hepatic recovery and persistent carcinogenic changes after MCLR toxicity in pre-existing NASH.

2021-11-06 | GSE188231 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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