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Links from GEO DataSets

Items: 13

1.

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [ATAC-seq]

(Submitter supplied) The lack of an appropriate preclinical model of non-alcoholic fatty liver disease (NAFLD) that recapitulates the whole disease spectrum impedes exploration of disease pathophysiology and the development of effective treatment strategies. Therefore, we developed new mose model with Streptozotocin (STZ)and high-fat diet (HFD). In breif, male C57BL/6J mice were injected with low-dose streptozotocin (40 mg/kg) for 5 consecutive days beginning at 7 weeks of age and subsequently fed a high-fat diet from week 8 (STZ+HFD) onwards. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21273
12 Samples
Download data: BED, BW
Series
Accession:
GSE246213
ID:
200246213
2.

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247 GPL21273
160 Samples
Download data: BED, BW
Series
Accession:
GSE246223
ID:
200246223
3.

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [RNA-seq]

(Submitter supplied) The lack of an appropriate preclinical model of metabolic dysfunction-associated steatotic liver disease (MASLD) that recapitulates the whole disease spectrum impedes exploration of disease pathophysiology and the development of effective treatment strategies. Considering the fact that MASLD patients accompanying type 2 diabetes mellitus (T2DM) have high risk of developing metabolic dysfunction-associated steatohepatitis (MASH), advanced fibrosis, and HCC, we treated low-dose streptozotocin (STZ; 40 mg/kg) for 5 consecutive days and subsequently fed a high-fat diet (HFD) to male C57BL/6J mice at 7 weeks of age (STZ+HFD). more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247
148 Samples
Download data: TXT
Series
Accession:
GSE246221
ID:
200246221
4.

RNA-seq of C3H/He mice on the American Lifestyle diet (ALIOS)

(Submitter supplied) We have developed a novel murine model of Diet-induced HCC via feeding the C3H/He mouse strain with the American life style diet (ALIOS) for 48 weeks. RNAseq was performed to the developed tumors as well as the non-tumor tissue of mice livers seeking for understanding the contributing pathways to the development and the progression of HCC in this mice strain. We also investigated whether the tumors developed in mice recaptiulate any particular human HCC subclass.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
50 Samples
Download data: TXT
Series
Accession:
GSE137407
ID:
200137407
5.

Induction of hepatocellular carcinoma through activation of stromal cells in Pdgf-c transgenic mice

(Submitter supplied) Liver cirrhosis is a strong risk factor for the development of hepatocellular carcinoma (HCC), yet the mechanisms by which cirrhosis predisposes patients to tumorigenesis are not well understood. Transgenic mice expressing platelet-derived growth factor C (Pdgf-c) under the control of the albumin promoter provide a unique animal model that mimics the step-wise disease progression in humans from fibrosis to HCC. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS5320
Platform:
GPL6246
16 Samples
Download data: CEL
Series
Accession:
GSE38199
ID:
200038199
6.
Full record GDS5320

Platelet-derived growth factor C transgenic model of hepatocellular carcinoma: liver stromal cells

Analysis of liver stroma from 8.8-week-old PDGF-C transgenics wherein PDGF-C is ectopically expressed in hepatocytes. The transgenics develop progressive liver fibrosis with a high incidence of HCC. Results provide insight into PDGF-C-driven molecular changes in liver stroma contributing to HCC.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 genotype/variation sets
Platform:
GPL6246
Series:
GSE38199
16 Samples
Download data: CEL
7.

Sex- and age-associated factors drive the pathophysiology of MASLD

(Submitter supplied) Metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly associated with obesity. The use of animal models fed Western-style diets is vital for investigating the molecular mechanisms contributing to metabolic dysregulation and for facilitating novel drug target identification. However, the sex- and age-associated mechanisms underlying the pathophysiology remain poorly understood. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
32 Samples
Download data: TXT
Series
Accession:
GSE274914
ID:
200274914
8.

A 5:2 intermittent fasting regimen initiated in the active phase ameliorates NASH, fibrosis and blunts HCC development via hepatic PPARα and PCK1

(Submitter supplied) The role and molecular mechanisms of intermittent fasting (IF) in non-alcoholic steatohepatitis (NASH) and its transition to hepatocellular carcinoma (HCC) are unknown. Here, we identified that an IF 5:2 regimen (two non-consecutive days of food deprivation per week), initiated in the active phase of mice, prevents NASH development as well as ameliorates established NASH and fibrosis without affecting total calorie intake. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
39 Samples
Download data: TSV, TXT
Series
Accession:
GSE255356
ID:
200255356
9.

Gene expression profile at single cell level of non-parenchymal cells from Fibrosis and Tumor (FAT) Metabolic Dysfunction-Associated Steatohepatitis (MASH) model vs healthy liver at 12- and 24-week timepoints.

(Submitter supplied) MASH is a subtype of metabolic dysfunction-associated steatotic liver disease, characterized by inflammation and fibrosis. Non-parenchymal cells in this dataset include mostly immune cells, as well as some other cell types like endothelial cells, cholangiocytes, stellate cells, etc.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: MTX, TSV
Series
Accession:
GSE261088
ID:
200261088
10.

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
11.

Identifying the role of Acox1 in metabolism and inflammation in non-alcoholic fatty liver disease through mRNA-sequencing.

(Submitter supplied) Purpose: To identify the impact of Acox1 on cellular metabolism and inflammation related to non-alcoholic fatty liver disease, within the context of obesogenic dietary stress. Methods: Hepatic mRNA profiles were obtained in triplicate for control and Acox1Lampe1 mice on chow diet or obesogenic diet. Profiles were generated using the Illumina HiSeq2000, reads that passed quality inspection were processed through the TopHap/Cufflinks pipeline. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: TXT
Series
Accession:
GSE89626
ID:
200089626
12.

A NEW PRECLINICAL MODEL OF WESTERN DIET-INDUCED PROGRESSION OF NON-ALCOHOLIC STEATOHEPATITIS TO HEPATOCELLULAR CARCINOMA

(Submitter supplied) Non-alcoholic steatohepatitis (NASH) results from accumulation of excessive liver lipids leading to hepatocellular injury, inflammation, and fibrosis that greatly increase the risk for hepatocellular carcinoma (HCC). Despite the well-characterized clinical and histological pathology for NASH-driven HCC in humans, its etiology remains unclear and there is a deficiency in pre-clinical models that recapitulate the progression of the human disease. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
6 Samples
Download data: TXT
Series
Accession:
GSE197884
ID:
200197884
13.

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
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