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ScRNAseq of hepatic CD11b positive immune cells from uninjured control (Ctrl) and liver fibrosis resolved (RES) mice

ABSTRACT: To explore key features associated with the resolution process in liver fibrosis, we here applied a previously reported murine liver fibrosis resolution model, in which wild-type mice were injected with carbon tetrachloride (CCl4) diluted in olive oil (1:9) intraperitoneally (0.6 μL/g body weight; Sigma) thrice per week for four weeks, and then observed without administration for 96 hours. We conformed that liver fibrosis was resolved in these mice (RES) after 96 hours from the last injection, along with upregulation of hepatic MMPs. Among CD45+ non-parenchymal cells, we noted that most MMPs were expressed by CD11b+ cells. To reveal the transcriptome profiling-based subtypes of CD45+ CD11b+ cells present during the liver fibrosis resolution, we performed scRNA-seq analysis. With corresponding cells from uninjured non-fibrotic wild-type mice as controls (Ctrl), a total of 7969 cells were clustered into 18 clusters based on the gene signatures. We revealed that a unique cluster of Ly6c2-low expressing CD11b+ macrophages (cluster Mac3) were enriched in livers resolved from CCl4-induced liver fibrosis. Comprehensive analysis of expression of known toll-like receptors in myeloid clusters demonstrated a unique upregulation of Tlr4 in Mac3. Moreover, only Ly6c2-low myeloid cells belonging to Mac 3 also demonstrated up-regulation of the expression of genes involved in extracellular matrix remodelling, post-phagocytosis, anti-inflammatory and antifibrotic pathways, and combined properties of both M1 and M2 features. Additionally, many of these genes highly expressed in Mac 3 were associated with the TLR4 pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE189606 | GEO | 2023/02/14

REPOSITORIES: GEO

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Expression data from murine hepatic stellate cells

Project description:Wnt/β-catenin is involved in every aspect of embryonic development and in the pathogenesis of many human diseases, and is also implicated in organ fibrosis. However, the role of β-catenin-mediated signaling on liver fibrosis remains unclear. To explore this issue, the effects of PRI-724, a selective inhibitor of the cAMP-response element-binding protein-binding protein (CBP)/β-catenin interaction, on liver fibrosis were examined using carbon tetrachloride (CCl4)- or bile duct ligation (BDL)-induced mouse liver fibrosis models. Following repetitive CCl4 administrations, the nuclear translocation of β-catenin was observed only in the non-parenchymal cells in the liver. PRI-724 treatment reduced the fibrosis induced by CCl4 or BDL, accompanied by the suppression of S100A4 expression, a CBP/β-catenin transcript. C-82, an active form of PRI-724, inhibited the activation of isolated primary mouse quiescent hepatic stellate cells (HSCs) and promoted cell death in culture-activated HSCs. During the fibrosis resolution period, an increase in F4/80+ CD11b+ and Ly6Clow CD11b+ macrophages was induced by CCl4 and was sustained for two weeks thereafter, even after having stopped CCl4 treatment. PRI-724 accelerated the resolution of CCl4-induced liver fibrosis, and this was accompanied by increased matrix metalloproteinase (MMP)-9, MMP-2, and MMP-8 expression in intrahepatic leukocytes. These results suggest that the inhibition of CBP/β-catenin suppresses liver fibrosis through the inhibition of HSCs activation, the induction of activated HSC death, and the production of MMPs from macrophages. Thus, targeting the CBP/β-catenin interaction may become a new therapeutic strategy in treating liver fibrosis. We used microarrays to detail the global change of gene expression by PRI-724 (C-82)-treatment in culture-activated murine hepatic stellate cells.

2018-09-30 | GSE73603 | GEO

RNAseq profiling of tumor, tumor-draining-lymph nodes, blood and tumor-associated macrophages of MC38 mice treated with the PI3Kg inhibitor AZD3458 and a combination of AZD3458 and anti-PD-1

Project description:RNAseq profiling of AZD3458 monotherapy and combination treatment with anti-PD-1 of whole tumors, isolated tumor macrophages (Mac) (CD45+CD11b+F4/80+), whole blood (PB) and tumor draining lymph nodes (TDLN) were assessed to elucidate further mechanisms leading to enhanced combination activity.

2021-02-28 | E-MTAB-10057 | biostudies-arrayexpress

RNA sequencing of WT and Hmgb2-/- mice liver treated with CCL4

Project description:loss of Hmgb2 in vivo in mouse liver largely prevented CCl4-induced liver fibrosis. The goal of the RNA-seq is to identify the Hmgb2 regulated genes in CCL4 induced liver fibrosis.

2019-10-01 | GSE98577 | GEO

MiR-29a regulates liver fibrosis

Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.

2015-03-31 | E-GEOD-67423 | biostudies-arrayexpress

Gene expression accompanying the promotion of hepatocellular carcinoma by intestinal microbiota and Tlr4 in mice.

Project description:The effect of Tlr4P712H mutation (rendering TLR4 non-functional), or gut-sterilization by antbiotics, on the induction of tumorgenesis by CCl4 and diethylnitrosamine (DEN) was characterized. Affymetrix Mouse 430 2.0 gene expression measurements were used to characterize the transcriptomic basis of the effects of the above treatments and genotypes on tumorgenesis. Gene expression of mouse livers of A. Normal liver from WT C3H/HeOuJ mice, B. HCC from WT C3H/HeOuJ mice treated with CCl4 and DEN, C.HCC from TLR4-mutant C3H/HeJ mice (Tlr4P712H) treated with CCl4 and DEN and D.HCC from WT C3H/HeOuJ mice treated with antibiotics (a combination of ampicillin (1 g/l), neomycin [1 g/l], metronidazole[1 g/l] and vancomycin [500 mg/l] in drinking water) and CCl4 and DEN were characterized.

2013-01-03 | E-GEOD-33446 | biostudies-arrayexpress

Carbon tetrachloride (CCl4) induced liver fibrosis

Project description:To understand the fibrotic response in the CCl4 induced liver fibrosis model, we performed RNA-seq of liver samples from mice treated with oil or CCl4.

2022-08-19 | GSE207855 | GEO

Expression anlysis of E10.5 yolk sac and E13.5 liver lineages from the wildtype mouse embryo

Project description:Single cell suspensions of E10.5 yolk sac cells and E13.5 fetal liver cells were purified by flow cytometry into the following immunophenotypically defined populations: (A) E10.5 diploid platelet-forming cells (megakaryocytic lineage, CD45-CD144-CD41high), E10.5 haematopoietic progenitor cells (CD45+CD41low), E10.5 myeloid cells (CD45+CD41low), and E10.5 endothelium (CD45-CD144+CD41-); and, (B) E13.5 megakaryocytes (CD61-enriched CD41+CD150+CD42D+), myeloid cells (CD45+CD11B+), and blast cells (CD45+CD11B-).

2014-07-27 | E-MTAB-2625 | biostudies-arrayexpress

Aberrant expression of microRNAs is associated to the progression of liver fibrosis

Project description:Establish the miRNA expression profile between advanced liver fibrosis and liver without fibrosis in mice Administrate CCL4 or olive oil in mouse twice a week first 4 weeks per peritoneum and then administrated once a week next four weeks. Mice were sacrificed on 4, 6, and 8 weeks.

2011-01-12 | E-GEOD-19865 | biostudies-arrayexpress

Expression data that were specifically regulated by lncRNA-HELF (ENSMUST00000147617 ) in livers of mice undergoing CCl4-induced liver fibrosis

Project description:Long non-coding RNAs (lncRNAs) are involved in numerous biological functions and pathological processes. In this study, we have identified a novel lncRNA ENSMUST00000147617, named Highly Expressed in Liver Fibrosis (lnc-HELF), which is remarkably up-regulated in mouse and human fibrotic livers. To identify the roles of lnc-HELF in liver fibrosis, we performed RNA-seq to analyze the effect of lnc-HELF deficient on CCl4-induced liver fibrosis. The mice were divided in three groups: mice treated with CCl4 in combination with injection of AAV8-NC (NC_CCl4, n=3), mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF1# (sh1_CCl4, n=3) and mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF2# (sh2_CCl4, n=3).

2023-10-05 | GSE182485 | GEO

A specific Peroxisome Proliferator-Activated Receptor (PPAR)-delta agonist is hepatoprotective and attenuates liver fibrogenesis

Project description:PPARδ is emerging as a key metabolic regulator with pleiotropic actions on various tissues including fat, skeletal muscle and liver. The aim of our study was to assess the effect of either the well-validated PPARδ agonist GW501516, or a novel PPARδ agonist KD3010 in mouse models of liver fibrosis. KD3010, but not GW501516, treated mice had markedly less liver injury induced by carbon tetrachloride (CCl4) injections. Deposition of extracellular matrix proteins was lower in the KD3010 group as compared to the vehicle or GW501516 treated group. Interestingly, profibrogenic CTGF was significantly induced by GW501516, but not KD3010, following CCl4 treatment. The hepatoprotective and antifibrotic effect of KD3010 was confirmed in a model of cholestasis-induced liver injury and fibrosis using bile duct ligation for three weeks. Hepatocytes were identified as targets for PPARδ agonist, and primary hepatocytes treated with KD3010 showed decreased serum starvation or CCl4-induced cell death, while GW501516 treated hepatocytes were not protected. KD3010 treatment of hepatocytes decreased reactive oxygen species (ROS) production after CCl4 exposure. In conclusion, our data demonstrate that a novel PPARδ agonist has hepatoprotective and antifibrotic effects in animal models of liver fibrosis. Given the oral availability and the favorable pharmacologic profile of KD3010, ligand activation of PPARδ represents an attractive and promising target for patients with chronic liver diseases. Total RNA was extracted from primary mouse hepatocytes treated with DMSO or PPARd agonists (KD3010, GW1516)

2012-04-18 | E-GEOD-32121 | biostudies-arrayexpress

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