Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RUNX1 mediating the effects of TGFβ stimulation in cholangiocytes

ABSTRACT: Cholestatic liver diseases, such as primary sclerosing cholangitis (PSC), are characterized by biliary fibroinflammation. Transforming growth factor-β (TGFβ) activated cholangiocytes release signals that recruit immune cells to drive inflammation and activate myofibroblasts to deposit the extracellular matrix (ECM). TGFβ signaling interacts with RUNX1 transcription factor. However, the role of RUNX1 has not been investigated in biliary fibroinflammation. Here we used mouse large biliary epithelial (MLE) cells that were treated with TGFβ (10ng/mL). ChIP-seq was performed followed by pathway analysis of genes associated with regions of RUNX1 binding.

ORGANISM(S): Mus musculus

PROVIDER: GSE306786 | GEO | 2025/09/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Affect of Aramchol on TGFβ stimulated H69 Cholangiocytes

Project description:Cholestatic liver diseases, such as primary sclerosing cholangitis (PSC), are characterized by biliary fibroinflammation. Transforming growth factor-β (TGFβ) activated cholangiocytes release signals that recruit immune cells to drive inflammation and activate myofibroblasts to deposit the extracellular matrix (ECM). TGFβ regulates stearoyl-CoA desaturase (SCD) in stimulating lipid signaling. However, the role of SCD or its inhibitor, Aramchol, has not been investigated in biliary fibroinflammation. Here we used human transformed H69 cholangiocytes that were treated with TGFβ (10ng/mL) with and without Aramchol acid (30µM) overnight. RNA-seq analysis showed significant inhibition of TGFβ-induced hepatic fibrosis pathways while upregulating peroxisome proliferator-activated receptor (PPAR) signaling by Aramchol.

2025-07-23 | GSE303012 | GEO

STAT3 protects from liver injury and fibrosis in a mouse model of sclerosing cholangitis

Project description:Background and aims: Signal transducer and activator of transcription 3 (Stat3) is the main mediator of interleukin-6 type cytokine signaling required for hepatocyte proliferation and hepatoprotection but its role in sclerosing cholangitis and other cholestatic liver diseases remains unresolved. Methods: We investigated the role of Stat3 in inflammation-induced cholestatic liver injury and used mice lacking the multidrug resistance gene 2 (mdr2-/-) as a model for SC. Results: We demonstrate that conditional inactivation of stat3 in hepatocytes and cholangiocytes (stat3 delta hc) of mdr2-/- mice strongly aggravated bile acid-induced liver injury and fibrosis. A similar phenotype was observed in mdr2-/- mice lacking IL-6 production. Biochemical and molecular characterization suggested that Stat3 exerts hepatoprotective functions in both, hepatocytes and cholangiocytes. Loss of Stat3 in cholangiocytes led to increased expression of TNFÎ± which might reduce the barrier function of bile ducts. Loss of Stat3 in hepatocytes led to upregulation of bile acid biosynthesis genes and downregulation of hepatoprotective epidermal growth factor receptor and insulin-like growth factor 1 signaling pathways. Consistently, stat3deltahc mice were more sensitive to cholic acid-induced liver damage than control mice. Conclusions: Our data suggest that Stat3 prevents cholestasis and liver damage in sclerosing cholangitis via regulation of pivotal functions in hepatocytes and cholangiocytes. Affymetrix microarray analyses was performed to identify metabolic and molecular pathways in stat3Dhc mdr2-/- mice that lead to cholestasis and bile acid-induced liver injury. To avoid false positive results that are due to differential cellular composition, we defined the onset of fibrosis and expression of fibrogenic factors in stat3Dhc mdr2-/- mice.

2010-10-20 | E-GEOD-18759 | biostudies-arrayexpress

STAT3 protects from liver injury and fibrosis in a mouse model of sclerosing cholangitis.

2010-10-20 | GSE18759 | GEO

RUNX1 mediating the effects of TGFβ stimulation in cholangiocytes

Project description:RUNX1 mediating the effects of TGFβ stimulation in cholangiocytes

| PRJNA1312110 | ENA

Common functional alterations identified in blood transcriptome of autoimmune cholestatic liver and inflammatory bowel diseases

Project description:Primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and inflammatory bowel diseases (IBDs), including Crohn’s disease (CD) and ulcerative colitis (UC), are heterogeneous chronic autoimmune diseases that may share underlying pathogenic mechanisms. Herein, we compared simultaneously analyzed blood transcriptomes from patients with PBC, PSC, and IBD.

2019-05-01 | GSE119600 | GEO

Comparison of extrahepatic cholangiocyte organoids and freshly isolated common bile duct cholangiocytes

Project description:Despite the impact of bile duct disorders, treatment options remain very limited. Poor access to biliary tissue and restrictions in long-term culture or significant expansion of primary cholangiocytes have posed major challenges for research in the field. These limitations have so far precluded large scale experiments such as transcriptomic and genome-wide analyses which are urgently needed to better understand biliary physiology and pathophysiology. To address this issue, we have developed a novel system for the isolation and propagation of primary cholangiocytes from the extrahepatic bile ducts. The resulting Extrahepatic Cholangiocyte Organoids (ECOs) maintain their genetic stability, transcriptomic profile and function over long term culture and are compatible with regenerative medicine applications such as biliary reconstruction. We established a novel protocol for the isolation and propagation of primary cholangiocytes from the extrahepatic biliary tree in the form of extrahepatic cholangiocyte organoids (ECOs). The aim of this experiment was to provide in depth characterisation of the transcriptome of ECOs during long term culture. We compare the transcriptome of ECOs cultured for 1 passage (P1), 10 passages (P10) and 20 passages (P20) with freshly isolated primary cholangiocytes from the common bile duct. Embryonic Stem Cells (ES) cells are used as a negative control=

2017-07-04 | E-MTAB-4591 | biostudies-arrayexpress

Downregulation of TGR5 (GPBAR1) in biliary epithelial cells is characteristic of sclerosing cholangitis and may contribute to disease pathogenesis

Project description:Primary sclerosing cholangitis (PSC) is characterized by chronic inflammation and progressive fibrosis of the biliary tree. The bile acid receptor TGR5 is found on biliary epithelial cells (BECs), where it promotes secretion, proliferation and tight junction integrity. Thus, we speculated that changes in TGR5 expression in BECs may contribute to PSC pathogenesis.

2021-03-12 | GSE168758 | GEO

RNA sequencing reveals differential MYC-driven gene expression as a driver of a divergent cholangiocyte response to stress

Project description:In Primary Sclerosing Cholangitis (PSC), some cholangiocytes undergo cell cycle arrest (senescence) while others proliferate (ductular reaction). Our aim was to determine the mechanisms driving this divergent response. We used lipopolysaccharide (LPS) to stress normal human cholangiocytes (NHC) transfected with a senescence reporter, p16- promoter driven green fluorescent protein. We performed RNA sequencing to assess gene expression profiles on non-senescent (GFP-) and senescent (GFP+) cholangiocytes. Our analysis revealed a MYC-driven gene expression profile in non-senescent cholangiocytes and suggest that MYC may function as a "molecular switch" in determining cholangiocyte responses to stress.

2025-07-30 | GSE296039 | GEO

Bulk RNA-seq in cholangiocytes from mouse model of primary biliary cholangitis

Project description:Bulk RNA-seq in cholangiocytes from mouse model of primary biliary cholangitis

| PRJNA836922 | ENA

Prominin-1-expressing Hepatic Progenitor Cells Induce Fibrogenesis in Murine Cholestatic Liver Injury

Project description:Purpose: Cholestatic liver injury is associated with intrahepatic biliary fibrosis, which can progress to cirrhosis. Resident hepatic progenitor cells (HPCs) expressing Prominin-1 (Prom1/CD133) become activated and participate in the expansion of cholangiocytes known as the ductular reaction. Previously, we demonstrated that in biliary atresia, Prom1(+) HPCs are present within developing fibrosis and that null mutation of Prom1 significantly abrogates fibrogenesis. Here, we hypothesized that these activated Prom1-expressing HPCs promote fibrogenesis in cholestatic liver injury. Methods: Using Prom1CreERT2-nLacZ/+;Rosa26Lsl-GFP/+ mice, we traced the fate of Prom1-expressing HPCs in the growth of the neonatal and adult livers and in biliary fibrosis induced by bile duct ligation (BDL). Results: Prom1-expressing cell lineage labeling with Green Fluorescent Protein (GFP) on postnatal day 1 exhibited an expanded population as well as bipotent differentiation potential towards both hepatocytes and cholangiocytes at postnatal day 35. However, in the adult liver, they lost hepatocyte differentiation potential. Upon cholestatic liver injury, adult Prom1-expressing HPCs gave rise to both PROM1(+) and PROM1(-) cholangiocytes contributing to ductular reaction without hepatocyte or myofibroblast differentiation. RNA-sequencing analysis of GFP(+) Prom1-expressing HPC lineage revealed a persistent cholangiocyte phenotype and evidence of Transforming Growth Factor-b pathway activation. Conclusion: Our data indicate that Prom1-expressing HPCs promote biliary fibrosis by activation of myofibroblasts in cholestatic liver injury.

2020-06-30 | GSE144726 | 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