Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular crosstalk between hepatocytes and hepatic stellate cells.

ABSTRACT: Aim of the study was to characterize at a molecular level (changes in transcriptomes) the crosstalk between tumor hepatocytes and activated hepatic stellate cells (HSC) in liver cancer. This was adressed by using a coculture model system of HepaRG cell line (tumor hepatocytes, human), and LX2 cell line (HSC, human). By using genome-wide expression profiling, we demonstrated that hepatocyte-HSC crosstalk is bidirectional and results in the deregulation of functionally relevant gene networks.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32565 | GEO | 2012/06/01

SECONDARY ACCESSION(S): PRJNA147123

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Molecular crosstalk between hepatocytes and hepatic stellate cells.

Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the crosstalk between tumor hepatocytes and activated hepatic stellate cells (HSC) in liver cancer. This was adressed by using a coculture model system of HepaRG cell line (tumor hepatocytes, human), and LX2 cell line (HSC, human). By using genome-wide expression profiling, we demonstrated that hepatocyte-HSC crosstalk is bidirectional and results in the deregulation of functionally relevant gene networks. HepaRG and LX2 cells were cultured alone in serum- and DMSO-free William's E medium or together using 1 M-BM-5m pore size transwell inserts which allow diffusion of media components but prevent cell migration (BD Biosciences, San Jose, CA). Triplicate experiments were performed: HepaRG (culture versus coculture), LX2 (culture versus coculture).

2012-05-31 | E-GEOD-32565 | biostudies-arrayexpress

Gene expression profiling of the human HepaRG hepatocellular carcinoma cell line under WNT3A stimulation.

Project description:The aim of the study was to characterize at a molecular level (changes in mRNA level) the effects of WNT3A on the human HepaRG hepatocellular carcinoma cell line. This was adressed by culturing HepaRG cells in presence or absence of Wnt3a.

2017-02-11 | GSE68633 | GEO

cGMP-dependent protein kinase 1 (cGK1) modulates human hepatic stellate cell activation

Project description:The activation of hepatic stellate cells (HSC) plays a crucial role in non-alcoholic fatty liver disease (NAFLD), which could further develop to non-alcoholic steatohepatitis (NASH) and liver fibrosis/cirrhosis. Since cGMP-dependent protein kinase 1 (cGK1) deficient (cGK1-KO) mice displayed hepatic insulin resistance we hypothesized that cGK1 modulates HSC activation and its metabolic consequences. First, retinol storage and gene expression were studied in cGK1-KO mice. Second, we investigated the effects of cGK1-silencing on gene expression in the human stellate cell line LX2. Finally, cGK1 expression was investigated in human liver biopsies covering a wide range of liver fat content. Retinyl-ester level in the liver of cGK1-KO mice was lower compared to wild-type animals, which was associated with increased inflammatory gene expression. mRNA regulation in cGK1-silenced LX2 cells showed stronger stellate cell activation profile, altered matrix degradation and elevated chemokine level. On the other hand, activation of LX2 cells suppressed cGK1 expression, which was associated with human data, showing a negative correlation between cGK1 mRNA and liver fat content in liver biopsies. These results suggest that the lack of cGK1 could possibly lead to stellate cell activation, which elevates chemokine expression and inflammatory processes, which in turn disturbs hepatic insulin sensitivity.

2018-09-11 | GSE111988 | GEO

Communication between the HCCLM3 cells and LX2 cells in a 3D tumor-on-a-chip

Project description:The communacation between the Hepatocellular carcinoma (HCC) and hepatic stellate cells(HSC) is not completely understood. Then a tumor-on-a-chip model was used to evaluate the crosstalk between the HCC cells (HCCLM3) and HSCs (LX2). After 5 days co-culture, we degraded the collagen hydrogel to isolate HCCLM3 cells and LX2 cells for RNA-seq.

2023-07-31 | GSE208007 | GEO

GENERATION OF HEPATIC STELLATE CELLS BY DIRECTED DIFFERENTIATION OF HUMAN PLURIPOTENT STEM CELLS

Project description:Hepatic stellate cells (HSC) are the main stromal cell component of the liver. In healthy liver, quiescent HSC participate in the homeostasis of extracellular matrix (ECM) and store vitamin A. Liver injury causes HSC activation, where they participate in the wound-healing response, by producing ECM components as well as cytokines involved in liver regeneration and inflammation. Moreover, HSC are the main cell type responsible for fibrosis progression. The lack of homogeneous cultures and renewable sources of human HSC has limited the studies of the role of HSC in liver injury, repair anf fibrosis. Here we report a procedure to direct the differentiation of human pluripotent stem cells (PSC) to HSC. The HSC–like population (iPS-HSC) was enriched in PDGFRβ positive cells that expressed key HSC markers. Whole genome transcriptomic analysis revealed that iPS-HSC displayed features intermediate to quiescent and activated HSC. Functional analysis demonstrated that iPS-HSC accumulated retinyl esters into lipid droplets and responded to injury mediators. Moreover, when cultured with HepaRG hepatocytes as aggregates, iPS-HSC support long-term hepatocyte metabolic function and respond to hepatocyte toxicity by activating and promoting organoid fibrogenesis.

2018-06-28 | GSE90525 | GEO

Expression data from human hepatic stellate cell line LX2 treated with suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA)

Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed gene expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.

2016-04-07 | E-MTAB-3764 | biostudies-arrayexpress

miRNA expression data from human hepatic stellate cell line LX2 treated with suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA)

Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA ) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed miRNA expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.

2019-07-20 | E-MTAB-6752 | biostudies-arrayexpress

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

Project description:RNA sequencing of LX2 cell line (a human hepatic stellate cell line). METTL3 overexpression or downreguation were achieved by lenti-virus transduction.

2022-07-13 | GSE207909 | GEO

FBP1 loss disrupts liver metabolism and promotes tumourigenesis through a hepatic stellate cell senescence secretome

Project description:Crosstalk between deregulated hepatocyte metabolism and cells within the tumour microenvironment, and consequent effects on liver tumourigenesis, are incompletely understood. We show here that hepatocyte specific loss of the gluconeogenic enzyme fructose 1,6-bisphosphatase 1 (FBP1) disrupts liver metabolic homeostasis and promotes tumour progression. FBP1 is universally silenced in both human and murine liver tumours, and hepatocyte-specific Fbp1 deletion results in steatosis, concomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-associated secretory phenotype (SASP). Depleting senescent HSCs by senolytic treatment with dasatinib/quercetin or ABT-263 inhibits tumour progression. We further demonstrate that FBP1-deficient hepatocytes promote HSC activation by releasing HMGB1; blocking its release with the small molecule inflachromene limits FBP1-dependent HSC activation, subsequent SASP development, and tumour progression. Collectively, these findings provide genetic evidence for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critical link between hepatocyte metabolism and HSC senescence that promotes tumour growth.

2020-03-02 | MSV000085045 | MassIVE

Gut-Liver Microphysiological Systems Revealed Arachidonic Acid as a Potential Crosstalk Factor Modulating Drug Metabolism

Project description:Coculture of hepatocytes with small intestine cells using MPS have been shown to enhance hepatic drug metabolism, yet the crosstalk mechanism is still unclear. Coculture of PXB-cells and iPS-derived intestine cells in MPS with perfusion and direct oxygenation were conducted to investigate this crosstalk. Analysis on albumin secretion, CYP enzyme actvity and differentially expressed genes confirmed that perfusion and direct oxygenation enhanced PXB-cells. Upregulation of "epoxygenase P450 pathway" GO terms indicated involvement of Arachidonic Acid (ARA) in the crosstalk mechanism. This is further confirmed by comparing the effect of ARA and coculture toward PXB-cells CYP enzymes activity. We hypothesize that some stimulus from PXB-cells resulted made iPS-derived intestine cells released ARA in form of lipoprotein, which is then taken in by PXB-cells and enhanced CYP activity.

2023-11-01 | GSE244407 | 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