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RNA-sequence data of liver sinusoidal endothelial cells in quiescent versus fibrotic and wild-type versus endothelial RBPj-deficent mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE120283 | GEO | 2020/04/01

REPOSITORIES: GEO

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RNA-sequence data of liver sinusoidal endothelial cells in quiescent versus fibrotic and wild-type versus endothelial RBPj-deficent mice

Project description:RNA-sequence data of liver sinusoidal endothelial cells in quiescent versus fibrotic and wild-type versus endothelial RBPj-deficent mice

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RNA-sequence data of liver sinusoidal endothelial cells from control and endothelial RBPj-deficent mice with liver fibrosis

Project description:Endothelial notch signaling dominantly regulates liver physiology and pathology. To further explore the role and mechanisms of endothelial notch in modulating development and progression of liver fibrogenesis, we established endothelial RBPj conditinal knock-out mice to specifically block notch activity in endothelium. After development of CCl4-induced liver fibrosis, SECs from control and RBPj knock-out mice were isolated and processed for RNA-seq.

2020-04-01 | GSE120282 | GEO

RNA-sequence data of liver sinusoidal endothelial cells in wild type and endothelial RBPj-conditional knock out (RBPjcKO) mice

Project description:The Notch pathway plays a critical role in regulating the proliferation and differentiation of endothelial cells during liver homeostasis, so we used EC-specific RBPj conditional knock out mice, and compared the gene expression profiles of LSECs isolated from wild type versus RBPjcKO mice.

2022-01-14 | GSE193424 | GEO

RNA-sequence data of liver sinusoidal endothelial cells from control and endothelial RBPj-deficent mice with liver fibrosis

Project description:RNA-sequence data of liver sinusoidal endothelial cells from control and endothelial RBPj-deficent mice with liver fibrosis

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Generation of Fibrotic Liver Organoids Using Hepatocytes, Primary Liver Sinusoidal Endothelial Cells, Hepatic Stellate Cells, and Macrophages.

Project description:Liver organoids generated with single or multiple cell types have been used to investigate liver fibrosis development, toxicity, pathogenesis, and drug screening. However, organoid generation is limited by the availability of cells isolated from primary tissues or differentiated from various stem cells. To ensure cell availability for organoid formation, we investigated whether liver organoids could be generated with cell-line-based Huh-7 hepatocellular carcinoma cells, macrophages differentiated from THP-1 monocytes, and LX-2 hepatic stellate cells (HSCs) and primary liver sinusoidal endothelial cells (LSECs). In liver organoids, hepatocyte-, LSEC-, macrophage-, and HSC-related gene expression increased relative to that in two-dimensional (2D)-cultured Huh-7/LSEC/THP-1/LX-2 cells without Matrigel. Thioacetamide (TAA) increased α-smooth muscle actin expression in liver organoids but not in 2D-cultured cells, whereas in TAA-treated organoids, the expression of hepatic and LSEC markers decreased and that of macrophage and HSC markers increased. TAA-induced fibrosis was suppressed by treatment with N-acetyl-L-cysteine or tumor-necrosis-factor-stimulated gene 6 protein. The results showed that liver toxicants could induce fibrotic and inflammatory responses in liver organoids comprising Huh-7/LSEC/macrophages/LX-2 cells, resulting in fibrotic liver organoids. We propose that cell-line-based organoids can be used for disease modeling and drug screening to improve liver fibrosis treatment.

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Capillarized Liver Sinusoidal Endothelial Cells Undergo Partial Endothelial-Mesenchymal Transition to Actively Deposit Sinusoidal ECM in Liver Fibrosis.

Project description:Tissue-specific endothelial cells are more than simply a barrier lining capillaries and are proved to be capable of remarkable plasticity to become active collagen matrix-producing myofibroblasts (MFs) in solid organs with fibrosis. Liver sinusoidal endothelial cells (LSECs) also participate in the development of hepatic fibrosis, but the exact roles and underlying mechanism have been poorly understood in addition to capillarization. In this study, we demonstrate, by using single-cell RNA sequencing, lineage tracing, and colocalization analysis, that fibrotic LSECs undergo partial endothelial mesenchymal transition (EndMT) with a subset of LSECs acquiring an MF-like phenotype. These phenotypic changes make LSECs substantial producers of extracellular matrix (ECM) preferentially deposited in liver sinusoids but not septal/portal scars as demonstrated by immunofluorescence in animal models and patients with fibrosis/cirrhosis, likely due to their limited migration. Bioinformatic analysis verifies that LSECs undergo successive phenotypic transitions from capillarization to mesenchymal-like cells in liver fibrosis. Furthermore, blockade of LSEC capillarization by using YC-1, a selective eNOS-sGC activator, effectively attenuates liver damage and fibrogenesis as well as mesenchymal features of LSECs, suggesting that capillarization of LSECs might be upstream to their mesenchymal transition during fibrosis. In conclusion, we report that capillarized LSECs undergo a partial EndMT characterized by increased ECM production without activating cell mobility, leading to perisinusoidal ECM deposition that aggravate liver function and fibrogenesis. Targeting this transitional process may be of great value for antifibrotic treatment of liver fibrosis.

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Hedgehog signalling regulates liver sinusoidal endothelial cell capillarisation.

Project description:Vascular remodelling during liver damage involves loss of healthy liver sinusoidal endothelial cell (LSEC) phenotype via capillarisation. Hedgehog (Hh) signalling regulates vascular development and increases during liver injury. This study therefore examined its role in capillarisation.Primary LSEC were cultured for 5 days to induce capillarisation. Pharmacological, antibody-mediated and genetic approaches were used to manipulate Hh signalling. Effects on mRNA and protein expression of Hh-regulated genes and capillarisation markers were evaluated by quantitative reverse transcription PCR and immunoblot. Changes in LSEC function were assessed by migration and tube forming assay, and gain/loss of fenestrae was examined by electron microscopy. Mice with acute or chronic liver injury were treated with Hh inhibitors; effects on capillarisation were assessed by immunohistochemistry.Freshly isolated LSEC expressed Hh ligands, Hh receptors and Hh ligand antagonist Hhip. Capillarisation was accompanied by repression of Hhip and increased expression of Hh-regulated genes. Treatment with Hh agonist further induced expression of Hh ligands and Hh-regulated genes, and upregulated capillarisation-associated genes; whereas Hh signalling antagonist or Hh ligand neutralising antibody each repressed expression of Hh target genes and capillarisation markers. LSEC isolated from Smo(loxP/loxP) transgenic mice that had been infected with adenovirus expressing Cre-recombinase to delete Smoothened showed over 75% knockdown of Smoothened. During culture, Smoothened-deficient LSEC had inhibited Hh signalling, less induction of capillarisation-associated genes and retention of fenestrae. In mice with injured livers, inhibiting Hh signalling prevented capillarisation.LSEC produce and respond to Hh ligands, and use Hh signalling to regulate complex phenotypic changes that occur during capillarisation.

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Liver sinusoidal endothelial cells - gatekeepers of hepatic immunity.

Project description:Liver sinusoidal endothelial cells (LSECs) line the low shear, sinusoidal capillary channels of the liver and are the most abundant non-parenchymal hepatic cell population. LSECs do not simply form a barrier within the hepatic sinusoids but have vital physiological and immunological functions, including filtration, endocytosis, antigen presentation and leukocyte recruitment. Reflecting these multifunctional properties, LSECs display unique structural and phenotypic features that differentiate them from the capillary endothelium present within other organs. It is now clear that LSECs have a critical role in maintaining immune homeostasis within the liver and in mediating the immune response during acute and chronic liver injury. In this Review, we outline how LSECs influence the immune microenvironment within the liver and discuss their contribution to immune-mediated liver diseases and the complications of fibrosis and carcinogenesis.

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RNA-sequence data of liver sinusoidal endothelial cells in wild type and endothelial RBPj-conditional knock out (RBPjcKO) mice

Project description:RNA-sequence data of liver sinusoidal endothelial cells in wild type and endothelial RBPj-conditional knock out (RBPjcKO) mice

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Immunological functions of liver sinusoidal endothelial cells.

Project description:Liver sinusoidal endothelial cells (LSECs) line the liver sinusoids and separate passenger leukocytes in the sinusoidal lumen from hepatocytes. LSECs further act as a platform for adhesion of various liver-resident immune cell populations such as Kupffer cells, innate lymphoid cells or liver dendritic cells. In addition to having an extraordinary scavenger function, LSECs possess potent immune functions, serving as sentinel cells to detect microbial infection through pattern recognition receptor activation and as antigen (cross)-presenting cells. LSECs cross-prime naive CD8 T cells, causing their rapid differentiation into memory T cells that relocate to secondary lymphoid tissues and provide protection when they re-encounter the antigen during microbial infection. Cross-presentation of viral antigens by LSECs derived from infected hepatocytes triggers local activation of effector CD8 T cells and thereby assures hepatic immune surveillance. The immune function of LSECs complements conventional immune-activating mechanisms to accommodate optimal immune surveillance against infectious microorganisms while preserving the integrity of the liver as a metabolic organ.

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