Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche (microarray)

ABSTRACT: Macrophages are strongly adapted to their tissue of residence. Yet, we know little about the cell-cell interactions that imprint the tissue-specific identities of macrophages in their respective niches. Using conditional depletion of liver Kupffer cells, we traced the developmental stages of monocytes differentiating into Kupffer cells and mapped the cellular interactions imprinting the Kupffer cell identity. Kupffer cell loss induced the tumor necrosis factor (TNF) and interleukin-1 (IL-1) receptor-dependent activation of stellate cells and endothelial cells, resulting in the transient production of chemokines and adhesion molecules orchestrating monocyte engraftment. Engrafted circulating monocytes transmigrated into the perisinusoidal space, and acquired the liver-associated transcription factors ID3 and LXRα. Coordinated interactions with hepatocytes induced ID3 expression, while endothelial cells and stellate cells induced LXRα via a synergistic NOTCH-BMP pathway. This study shows that the Kupffer cell niche is composed of stellate cells, hepatocytes and endothelial cells that together imprint the liver-specific macrophage identity.

ORGANISM(S): Mus musculus

PROVIDER: GSE135788 | GEO | 2019/08/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche (RNA-Seq)

Project description:Macrophages are strongly adapted to their tissue of residence. Yet, we know little about the cell-cell interactions that imprint the tissue-specific identities of macrophages in their respective niches. Using conditional depletion of liver Kupffer cells, we traced the developmental stages of monocytes differentiating into Kupffer cells and mapped the cellular interactions imprinting the Kupffer cell identity. Kupffer cell loss induced the tumor necrosis factor (TNF) and interleukin-1 (IL-1) receptor-dependent activation of stellate cells and endothelial cells, resulting in the transient production of chemokines and adhesion molecules orchestrating monocyte engraftment. Engrafted circulating monocytes transmigrated into the perisinusoidal space, and acquired the liver-associated transcription factors ID3 and LXRα. Coordinated interactions with hepatocytes induced ID3 expression, while endothelial cells and stellate cells induced LXRα via a synergistic NOTCH-BMP pathway. This study shows that the Kupffer cell niche is composed of stellate cells, hepatocytes and endothelial cells that together imprint the liver-specific macrophage identity.

2019-08-14 | GSE135789 | GEO

Liver cells study

Project description:To characterise liver cells from wt, untreated adult male mice. In particular we are interested on hepatocytes (HCs), hepatic stellate cells (HSCs), liver sinuisoidal endothelial cells (LSECs), Kupffer cells (KCs) and cholangiocytes (CHs).

2023-05-24 | GSE222597 | GEO

Qualifying a human Liver-Chip for predictive toxicology: Performance assessment and economic implications

Project description:We assess RNA expression in human primary hepatocytes in Vials Day 0 and Liver-Chips on Day 3 and Day 7 for two different donors. The hepatocytes were co-cultured in Liver-Chip model with Kupffer cells and Liver sinusoidal endothelial cells (LSECs) and stellate cells .

2022-10-14 | GSE207339 | GEO

Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche

Project description:Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche

| PRJNA560060 | ENA

Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche (microarray)

Project description:Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche (microarray)

| PRJNA560062 | ENA

Expression data of liver resident cells from C57BL/6 mouse

Project description:The liver is composed of various resident cells, including hepatocytes, Kupffer cells, liver sinusoidal endothelial cells (LSEC), and hepatic stellate cells (HSC). Hepatocytes are the primary type of liver cells, constituting 80% of the liver's mass, and are responsible for tasks such as protein and lipid synthesis, detoxification, and bile secretion. Kupffer cells, on the other hand, are liver-resident macrophages that play a crucial role in detecting foreign antigens and danger signals within the liver, as well as clearing apoptotic cells. LSEC is in charge of blood vessel formation in the liver and is responsible for eliminating cell debris. In the quiescent state, HSC stores vitamin A and is essential in liver fibrosis when activated. Freshly isolated HSCs undergo automatic activation upon culture. In this study, we present microarray data for freshly isolated mouse hepatocytes, Kupffer cells and LSEC, along with HSCs that have been cultured for 1, 7 or 14 days.

2023-02-27 | GSE226103 | GEO

Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche (RNA-Seq)

Project description:Stellate cells, hepatocytes and endothelial cells imprint the Kupffer cell identity on monocytes colonizing the liver macrophage niche (RNA-Seq)

| PRJNA560063 | ENA

Human liver cells proteome

Project description:The human liver functions through a complex interplay of parenchymal and non-parenchymal cells, which participate in performing many essential aspects of metabolism and secretion. Mass spectrometry-based proteomic analysis of intact tissue has improved the understanding of these processes, by providing an in-depth view of the human liver proteome. However, the predominance of parenchymal cells, i.e. hepatocytes, means that the total tissue proteome mainly reflects hepatocyte expression. In this study, we therefore used quantitative label-free proteomic analysis to analyze the proteomes of the major parenchymal and non-parenchymal cell types in the human liver, i.e. hepatocytes, liver sinusoidal endothelial cells, Kupffer cells, and hepatic stellate cells. We found that our data recapitulated specific functional differences between cell types, meaning that it can be used to reliably probe various aspects of cellular interplay. Thus, the data we provide constitutes a unique resource for exploring the human liver proteome at major cell type resolution.

2020-04-09 | PXD012615 | Pride

GFP and mCherry gene expression at single cell level of all liver cell types from B6J mice

Project description:Diacylglycerol acyltransferase (DGAT)-2 catalyzes the final step of triglyceride (TG) synthesis. DGAT2 deletion in mice lowers liver TGs and DGAT2 overexpression might have the opposite effect. Mouse DGAT2 was overexpressed in C57Bl/6J mice using adeno-associated virus 8 (AAV8 and AAV-DJ). The tissue specificity of AAV8 and AAV-DJ was first evaluated. To confirm that AAV8 and AAV-DJ only infected hepatocytes and not other cells in liver, we carried out single cell sequencing of liver cells isolated from mice infected with AAV8-mCherry and AAV-DJ-GFP. The mCherry and GFP signals were highly expressed in hepatocytes and not in stellate, endothelial, or Kupffer cells.

2024-01-30 | GSE250338 | GEO

Liver-derived signals sequentially reprogram myeloid enhancers to initiate and maintain Kupffer cell identity (ATAC-Seq)

Project description:Tissue environment plays a powerful role in establishing and maintaining the distinct phenotypes of resident macrophages, but the underlying molecular mechanisms remain poorly understood. Here, we characterized transcriptomic and epigenetic changes in repopulating liver macrophages following acute Kupffer cell depletion as a means to infer signaling pathways and transcription factors that promote Kupffer cell differentiation. We obtain evidence that combinatorial interactions of the Notch ligand DLL4 and transforming growth factor-b (TGF-β) family ligands produced by sinusoidal endothelial cells and endogenous LXR ligands were required for the induction and maintenance of Kupffer cell identity. DLL4 regulation of the Notch transcriptional effector RBPJ activated poised enhancers to rapidly induce LXRα and other Kupffer cell lineage-determining factors. These factors in turn reprogrammed the repopulating liver macrophage enhancer landscape to converge on that of the original resident Kupffer cells. Collectively, these findings provide a framework for understanding how macrophage progenitor cells acquire tissue-specific phenotypes.

2019-10-08 | GSE128659 | 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