Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNA sequencing of liver biopsy-derived organoids from patients with alcohol-associated liver disease and paired tissues

ABSTRACT: Bulk RNA sequencing of liver biopsy-derived organoids from patients with alcohol-associated liver disease and paired tissues

PROVIDER: PRJNA1134631 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Bulk RNA sequencing of liver biopsy-derived organoids from patients with alcohol-associated liver disease and paired tissues

Project description:RNA sequencing was performed on liver organoids obtained from biopsies (b-Orgs) and paired tissues collected at different stages of alcohol-associated liver disease (ALD) using biliary (BEC) and hepatocyte (HEP) culture conditions. Different "generations" and passages of b-Orgs cultured with HEP medium were also sequenced. Besides, sequencing was also performed on vehicle and b-Orgs treated with Alcohol-associated hepatitis (AH)-medium. Finally, standard cholangiocyte organoids (Chol-Orgs) generated by dissociation of end-stage liver resections from ALD patients were sequenced.

2025-08-28 | GSE272014 | GEO

Modeling Tumor Development and Metastasis using Paired Organoids Derived from Patients with Colorectal Cancer Liver Metastases

Project description:Tumor metastasis accounts for the majority of cancer-related deaths; it is therefore important to develop preclinical models that faithfully recapitulate disease progression. Here, we generated paired organoids derived from primary tumors and matched liver metastases in the same colorectal cancer patients (CRC). Despite the fact that paired organoids exhibit comparable gene expression and cell morphology. organoids from metastatic lesions demonstrate more aggressive phenotypes, tumorigenesis, and metastatic capacity than those from primary lesions. Transcriptional analyses of the paired organoids reveal signature genes and pathways altered during the progression of CRC. including SOX2, altered during the progression of CRC. Further study shows that inducible knockdown of SOX2 attenuated invasion, proliferation, and liver metastasis outgrowth. Taken together, we use patient-derived organoids to model cancer metastasis. Our data propose that SOX2 is not only a critical biomarker for the development and metastasis of CRC, but also a potent target for the disease treatment.

2020-10-05 | GSE148918 | GEO

Patient-derived liver organoids recapitulate epithelial heterogeneity and enable precision disease modelling of alcohol-associated liver disease

Project description:Organoids are emerging as a powerful human-based in vitro tool in the biomedical field. However, patient-derived liver organoids fail to recapitulate the liver epithelial heterogeneity and its generation still requires liver surgical resections, thus limiting personalized chronic liver diseases modeling. Here, we report the derivation of organoids from intact liver needle biopsies(b-Orgs) from alcohol-associated liver disease (ALD) patients for precision disease modeling and drug testing. B-Orgs were generated with an efficiency of 80% from patients with early and advanced stages of ALD. b-Orgs show an enriched hepatocyte phenotype as assessed by immunofluorescence, functional studies, and transcriptomics. Single cell RNA-sequencing revealed a heterogeneous epithelial composition comprising hepatocyte, biliary and progenitor hepatobiliary populations, mirroring the epithelial populations found in advanced ALD patients. Moreover, b-Orgs preserve disease-stage features, as b-Orgs from advanced ALD patients showed increased expression of genes related to epithelial-mesenchymal transition, angiogenesis and inflammation. Stimulation of b-Orgs with ethanol and pro-inflammatory mediators,promoted ALD features such asROS production, lipid accumulation, inflammation and decreased proliferation, which were mitigated in response to prednisolone. Overall, we provide a new methodology to obtain b-Orgs showing epithelial complexity and patient specific features, thus expanding organoid-based liver disease modelling for personalized medicine.

2026-01-02 | GSE273146 | GEO

Blockade of lL17 signaling reverses alcohol-induced liver injury, and excessive alcohol drinking in mice.

Project description:Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.

2020-04-07 | GSE137228 | GEO

Liver of alcohol-treated mouse

Project description:Liver of alcohol-treated mouse

| PRJNA782325 | ENA

Expression data from Human liver biopsy

Project description:Expression data from Human liver biopsy

| PRJNA690119 | ENA

Liver macrophage changes during early adaptation to alcohol exposure

Project description:Liver macrophages consist of both Kupffer cells (KCs) and infiltrating macrophages (IM), and both populations change during alcohol associated liver disease. It has been suggested that KCs undergo a pro-inflammatory change after alcohol exposure, but the extent to which a pro-inflammatory shift results from IMs rather than KC activation is unclear. The purpose of this study was to examine the early effects of alcohol exposure on KCs and IMs in a murine model and compare these effects to observations in human liver. Mice were fed the Lieber-Decarli ethanol diet and total liver macrophage, and KC specific phenotypes were examined by flow cytometry, ex vivo cell culture and KC single cell RNAseq. Liver tissues from autopsy and transplant patients with different alcohol phenotypes were assessed. Early alcohol exposure caused a shift in the properties of total liver macrophages with an initial pro-inflammatory effect that partially resolved by 10 days. KCs became steadily less inflammatory over the first 10 days of alcohol exposure. Alcohol exposure in the absence of liver disease also shifted macrophage phenotypes in human livers. These results show that early alcohol exposure is sufficient to cause KC adaptation in a way that maintains liver homeostasis and limits inflammation. Understanding the mechanisms of these changes and how to sustain them may help prevent the development of long-term liver injury.

2025-11-17 | GSE310021 | GEO

Patient-derived liver organoids recapitulate epithelial heterogeneity and enable precision disease modelling of alcohol-associated liver disease

Project description:Patient-derived liver organoids recapitulate epithelial heterogeneity and enable precision disease modelling of alcohol-associated liver disease

| PRJNA1140246 | ENA

Epigenome analysis of brochoscopic paired biopsy specimens from tumoral sites and the contralateral bronchus.

Project description:Genome wide DNA methylation profiling of brochoscopic paired biopsy samples from tumoral sites and the contralateral bronchus (controls). The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in bronchoscopic biopsy samples. In 37 patients (74 samples) a difinite histological diagnosis could be reached. In the remaining 36 samples the diagnosis remained indefinite, the assumption of the pathologists is stated.

2021-03-02 | GSE158075 | GEO

Alcohol feeding promotes colonic permeability and changes in colonic organoid stem cell fate

Project description:Alcohol increases intestinal permeability to pro-inflammatory microbial products including endotoxin and this is a key step in alcohol-induced organ damage such as alcoholic liver disease. Elevated intestinal permeability is observed even after a period of sobriety. We sought to investigate mechanisms contributing to long-term effects of alcohol on intestinal permeability by testing the hypothesis that alcohol affects intestinal stem cells using ex vivo organoids generated from jejunum and colon from chronic alcohol fed mice.

2018-02-14 | GSE99291 | 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