Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of hiHepPCs in various culture conditions, human liver-derived hepatocytes, human liver-derived cholangiocytes, HUVECs, and HPBECs

ABSTRACT: Transcriptome analysis of hiHepPCs in various culture conditions, human liver-derived hepatocytes, human liver-derived cholangiocytes, HUVECs, and HPBECs

PROVIDER: PRJNA494323 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7948890.fastq.gz	Fastqsanger.gz
	SRR7948900.fastq.gz	Fastqsanger.gz
	SRR7948891.fastq.gz	Fastqsanger.gz
	SRR7948901.fastq.gz	Fastqsanger.gz
	SRR7948892.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 25

Similar Datasets

Transcriptome analysis of hiHepPCs in various culture conditions, human liver-derived hepatocytes, human liver-derived cholangiocytes, HUVECs, and HPBECs

Project description:Transcriptome analysis of human induced hepatic progenitor cells (hiHepPCs) in various culture conditions, human liver-derived hepatocytes, human liver-derived cholangiocytes, human umbilical vein endothelial cells (HUVECs), and human peripheral blood-derived endothelial cells (HPBECs) We found that a specific combination of three transcription factors, FOXA3, HNF1A, and HNF6, could convert HUVECs and HPBECs into cells that closely resembled hepatic progenitor cells in vitro. These hiHepPCs were expandable in long-term culture and able to differentiate into hepatocytes and cholangiocytes in accordance with their culture conditions. We conducted RNA-seq analyses to investigate the characteristincs of hiHepPCs and their progenies, in addition to those of parental HUVECs, HPBECs, and human liver-derived cells.

2020-08-12 | GSE120732 | GEO

Generation of functional ciliated cholangiocytes from human pluripotent stem

Project description:We report on the successful generation of functional ciliated cholangoocytes from hPSCs that will provide new opportunities to study and treat diseases of the liver. Both monolayer- and organoid-derived cells are adaptable for further bioengineering approcahes to produce more complex hPSC-deived liver tissue with biliary ductal structures. Additionally, the successful engraftment of differentiated cholangiocytes in the liver of immune-imcompetent mice provides the basis for developing novel therapeutic strategies to treat cholangiopathies.

2021-10-03 | GSE175502 | GEO

Targeting UBC9-mediated Protein Hyper-SUMOylation in Cystic Cholangiocytes Halts Polycystic Liver Disease in Experimental Models

Project description:Background & Aims: polycystic liver diseases (PLDs) are genetic disorders characterized by progressive development of multiple fluid-filled biliary cysts. Most PLD-causative genes participate in protein biogenesis and/or transport. Post-translational modifications (PTMs) are implicated in protein stability, localization and activity, contributing to human pathobiology; however, their role in PLD is unknown. Here, we aimed to unveil the role of protein SUMOylation in PLD and its potential therapeutic targeting. Methods: levels and function of SUMOylation, along with response to S-adenosylmethionine (SAMe, inhibitor of the SUMOylation enzyme UBC9) and/or short-hairpin RNAs (shRNAs) against UBE2I (UBC9), were evaluated in vitro, in vivo and/or in patients with PLD. SUMOylated proteins were determined by immunoprecipitation and proteomic analyses by mass spectrometry. Results: most SUMOylation-related genes were found overexpressed (mRNA) in polycystic human and rat liver tissue, as well as in cystic cholangiocytes in culture compared to controls. Increased SUMOylated protein levels were also observed in cystic human cholangiocytes in culture, which decreased after SAMe administration. Chronic treatment of polycystic (PCK: Pkdh1-mut) rats with SAMe halted hepatic cystogenesis and fibrosis, and reduced liver/body weight ratio and liver volume. In vitro, both SAMe and shRNA-mediated UBE2I knockdown increased apoptosis and reduced cell proliferation of cystic cholangiocytes. High-throughput proteomic analysis of SUMO1-immunoprecipitated proteins in cystic cholangiocytes identified candidates involved in protein biogenesis, ciliogenesis and proteasome degradation. Accordingly, SAMe hampered the proteasome hyperactivity in cystic cholangiocytes, leading to the activation the unfolded protein response (UPR) and stress-related apoptosis.

2020-09-29 | PXD021140 | Pride

Targeting UBC9-mediated Protein Hyper-SUMOylation in Cystic Cholangiocytes Halts Polycystic Liver Disease in Experimental Models

2020-09-29 | PXD021139 | Pride

MiRNA expression in embryonic murine hepatocytes versus murine cholangiocytes at E18.5

Project description:Differentially expressed miRNAs between hepatocytes (GFP-neg in SOX9-GFP mice) and cholangiocytes (GFP-pos in SOX9-GFP mice) in mice at E18.5. We want to compare miRNA population in biliary cells and parenchymal cells (depleted from hematopoietic cells) during liver development. Cholangiocytes specifically express the transcription factor Sox9. This enables to separate cholangiocytes from the rest of the liver parenchyma by FACS from Sox9-GFP transgenic mice. In conclusion, we want to compare miRNA population in our GFP+ cells (cholangiocytes) and our GFP- cells (liver parenchyma depleted from hematopoietic cells).

2018-12-20 | GSE100145 | GEO

Cholangiocytes contribute to hepatocyte regeneration after partial liver injury in larval zebrafish

Project description:Liver possesses robust regenerative ability, characterized by flexibility in the cellular source of regeneration based on the extent of the injury. After partial hepatectomy or minor injuries, hepatocytes, the primary liver cells, undergo self-duplication to replenish the liver mass. In contrast, when the damage is extensive, or hepatocyte proliferation is impaired, cholangiocytes contribute to hepatocyte recovery. This current paradigm of regenerative flexibility in the liver has been established for animals with little or no growth. However, the regenerative mechanisms during periods of growth in young animals remain unexplored. Here, we establish two new partial liver injury protocols in the zebrafish model of rapid growth during late larval stage and observe emergence of de novo hepatocytes in the presence of spared hepatocytes. Using single-cell RNA sequencing and lineage tracing, we identify cholangiocytes as the source of de novo hepatocytes. Our study offers a new perspective on the current paradigm of liver regenerating by proposing cholangiocyte-to-hepatocyte transdifferentiation as the default mechanism of hepatocyte recovery in late larval stage zebrafish.

2024-11-13 | GSE272484 | GEO

Transcriptome analysis of embryonic cholangiocytes

Project description:Purpose: The aim of this study is to propose a computational model which can help in unravelling the mechanisms of initial bile duct lumen formation. Guided by the quantification of morphological features and expression of genes in developing bile ducts (cholangiocytes) from embryonic mouse liver, hypotheses for the mechanisms of biliary lumen formation were generated and tested with the model. Here, the RNA-sequencing data were collected from purified embryonic cholangiocytes at two developmental stages (E16 and E18).

2021-05-31 | GSE163062 | GEO

Generation of functional cholangiocytes from human pluripotent stem cells and HepaRG cells

Project description:Gene expression profile analysis allowed to identify a panel of genes and pathways characteristic of hESC-and HepaRG-derived cholangiocytes.

2013-10-28 | GSE51791 | GEO

Transcriptome analysis of liver tumors derived from human induced liver cancer-forming cells (iLCCs)

Project description:We found that a set of six transcription factors, FOXA3, HNF1A, HNF1B, LIN28B, L-MYC, and KLF5, can induce direct conversion of human umbilical vein endothelial cells (HUVECs) into liver cancer-forming cells (LCCs). These induced LCCs (iLCCs) efficiently give rise to tumors that closely resemble human combined hepatocellular cholangiocarcinoma after transplantation to immunodeficient mice. We conducted RNA-seq analyses to investigate the characteristincs of the tumors derived from iLCCs.

2022-02-27 | GSE184539 | GEO

Interaction with Cholangiocytes and Neutrophils

Project description:Alcoholic hepatitis (AH) is a life-threatening disease with limited treatment options. The presence of cholestasis worsens prognosis but the responsible mechanism is unknown. AH results in infiltration of polymorphonuclear neutrophils (PMNs) in the liver, and cholestasis often reflects bile duct pathology, so we investigated whether and how PMNs interact with cholangiocytes in AH.

2020-03-13 | GSE146899 | 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