Single Cell RNAseq analysis of mouse NASH liver cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA865800 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20818233_1.fastq.gz | Fastqsanger.gz | |||
| SRR20818233_2.fastq.gz | Fastqsanger.gz | |||
| SRR20818234_1.fastq.gz | Fastqsanger.gz | |||
| SRR20818234_2.fastq.gz | Fastqsanger.gz |
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Project description:The liver is undergoing major rearrangements during the development of non-alcoholic steatohepatitis (NASH), from steatosis to severe lipid accumulation, inflammation and fibrosis. The mechanisms for this transition and the molecular changes preceding NASH are not fully understood. Here, we perform a single-cell RNA sequencing survey of 13,240 mouse liver cells during the development of non-alcoholic fatty liver disease. By measuring the entire transcriptome on a single-cell level from mice in the early stages of NASH development, we recognize known hepatocyte cell populations, Kupffer cells and stellate cells, as well as distinct gene expression changes in hepatocytes. We also reveal high hepatocyte heterogeneity in steatosis markers which projects a lipogenic trajectory of known and novel steatosis-associated genes. Importantly, we uncover distinct clusters of hepatocytes characterized by high or low Srebp1c expression with unique molecular signatures of lipogenesis. These results identify a novel regulatory pathway for lipogenesis in the liver that contributes to NASH progression.
2022-08-06 | GSE210501 | GEO
Project description:Human genetic studies have identified several MARC1 variants as protective against non-alcoholic fatty liver diseases (NAFLD). The MARC1 variants are associated with reduced lipid profiles, liver enzymes, and liver-related mortality. However, the role of mitochondrial amidoxime reducing component 1 (mARC1), encoded by MARC1, in NAFLD is still unknown and the therapeutic potential of this target has never been developed. Given that mARC1 is mainly expressed in hepatocytes, we developed an N-acetylgalactosamine conjugated mouse mARC1 siRNA to address this. In ob/ob mice, knockdown of mARC1 in mouse hepatocytes resulted in decreased liver weight, serum lipid enzymes, low-density lipoprotein cholesterol, and liver triglycerides. Loss of mARC1 also improved the lipid profiles and attenuated liver pathological changes in two diet-induced nonalcoholic steatohepatitis (NASH) mouse models. A comprehensive analysis of mARC1-deficient liver in NASH by metabolomics, proteomics, and lipidomics showed that mARC1 knockdown partially restored metabolites and lipids altered by diets. Taken together, loss of mARC1 protects mouse liver from NASH, suggesting a potential therapeutic approach of NASH by downregulation of mARC1 in hepatocytes.
2023-04-28 | MSV000091820 | MassIVE
Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays
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Project description:Comparison between livers of FLS mice and livers of DS (DD shionogi) mice We used FLS mice as model animals of human NASH, while DS mice as control animals. FLS mice develops NASH spontaneously. DS mouse strain is a sister strain of the FLS mouse strain. We compared RNA from pooled livers of three FLS mice and three DS mice at 19 weeks. NASH in livers from FLS mice was confirmied pathologically while simple steatosis of DS mouse livers confirmed.
2013-03-30 | E-GEOD-45624 | biostudies-arrayexpress
Project description:Single-Cell Analysis of NASH mouse livers
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Project description:Gene expression profiling reveals a potential role of isorhamnetin in the mitigation of NASH features including steatosis, liver injury, and fibrosis Microarray gene expression profiling was conducted for technical replicates of healthy liver as control (CTL), NASH-induced (NASH), NASH-induced treated with isorhamnetin for 14 days (50 mg/kg of body weight) (NASH+ISO) liver tissues to identify its effect in the regulation of pathways involved in pathologic features of NASH.
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Project description:Single-nucleus RNA-seq of NASH HCC liver tissue
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Project description:Non-alcoholic steatohepatitis (NASH) is the most significant cause of chronic liver disease worldwide, with limited therapeutic options. In this experiment, a choline-deficient amino acid-defined high fat diet (CDAHFD) were used to construct a mouse NASH model. After 16 weeks of CDAHFD diets, liver samples were collected. We want to further confirm that the elevated EFHD2 is specifically expressed in infiltrated macrophages/monocytes in NASH.
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Project description:Non-alcoholic fatty liver disease (NAFLD) is a leading form of chronic liver disease with large unmet need. Non-alcoholic steatohepatitis (NASH), a progressive variant of NAFLD, can lead to fibrosis, cirrhosis, and hepatocellular carcinoma. To identify potential new therapeutics for NASH, we used a computational approach based on Connectivity Map (CMAP) analysis, which pointed us to a potential application of bromodomain and extra-terminal motif (BET) inhibitors for treating NASH. To experimentally validate this hypothesis, we tested a small-molecule inhibitor of the BET family of proteins, GSK1210151A (I-BET151), in the STAM mouse NASH model at two different dosing timepoints (onset of NASH and onset of fibrosis) to assess its potential effectiveness for the treatment of NASH and liver fibrosis. I-BET151 decreased the non-alcoholic fatty liver disease activity score (NAS), a clinical endpoint for assessing the severity of NASH, as well as progression of liver fibrosis and interferon-γ expression. Transcriptional characterization through RNA-sequencing pointed to alterations in molecular mechanisms related to interferon signaling and cholesterol biosynthesis following treatment, as well as reversal of gene expression patterns linked to fibrotic markers. Altogether, these results suggest that inhibition of BET proteins may present a novel therapeutic opportunity in the treatment of NASH and liver fibrosis.
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Project description:The transcription factor NRF2 and its negative regulator KEAP1 are master regulators of redox, metabolic and protein homeostasis, detoxification and appear therefore as attractive drug targets for the treatment of NASH. S217879 a small molecule disrupting the KEAP1-NRF2 interaction has been highly characterized using various molecular and cellular assays. It was then evaluated in two different NASH-relevant preclinical models, and RNAseq data were obtained with samples from Diet-induced Obesity NASH (DIO NASH) mouse model. In DIO NASH mice, S217879 treatment resulted in a significant improvement of established liver injury with clear reduction in both NAS score as well as liver fibrosis. Alpha SMA and Col1A1 staining as well as quantification of liver hydroxyproline levels confirmed the reduction in liver fibrosis in response to S217879. RNA seq analyses revealed major alterations in the liver transcriptome in response to S217879 with activation of NRF2-dependent gene transcription as well as a marked inhibition of key signaling pathways driving disease progression
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