Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227797 | ENA |
REPOSITORIES: ENA
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Project description:Metabolomic analysis on hepatic stellate cells isolated from PBS- or thioacetamide (TAA)-treated wild-type and Cyp1b1 knockout mice was performed to determine the metabolic basis by which CYP1B1 ablation inhibits HSC activation and liver fibrosis.
2024-08-28 | MSV000095716 | MassIVE
Project description:Hepatic stellate cells are involved in the development of hepatic fibrosis. We here perform transcriptional profiling of hepatic stellate cells (HSCs) isolated from Western diet/high fructose-fed C57BL6/J mice, carbon tretrachloride (CCl4)-treated C57BL6/J mice, and of murine HSCs differentiated in vitro. Specifically, gene expression profiles are obtained from hepatic stellate cells isolated from C57BL6 mice fed a Western Diet supplemented with high fructose for 12, 16 or 24 weeks or normal chow. From hepatic stellate cells isolated from C57BL6 mice treated CCl4 for 1, 4 or 8 weeks or treated with vehicle. From hepatic stellate cells isolated from healthy C57BL6 mice and seeded on normal plastic cell culture dishes for 1, 4, 8, or 12 days. And from hepatic stellate cells isolated from healthy C57BL6 mice and seeded on normal plastic cell culture dishes for 6 days in the presence of 10uM U0126 or DMSO.
2019-04-07 | E-MTAB-7054 | biostudies-arrayexpress
Project description:Background & Aims: Rapid induction of beta-PDGF receptor (beta-PDGFR) is a core feature of hepatic stellate cell activation, the hallmark of liver fibrogenesis. However, biological consequences of the induction are not well characterized. We aimed to determine the involvement of beta-PDGFR-mediated molecular pathway activation on hepatic stellate cells in liver injury, fibrogenesis, and carcinogenesis in vivo. Methods: Loss and constitutive activation of beta-PDGFR were assessed in mouse models with either a stellate cell-specific beta-PDGFR knockout or the expression of an autoactivating mutation respectively. Liver injury and fibrosis were induced in two mechanistically distinct models: carbontetrachloride (CCl4) treatment and ligation of the common bile duct. Hepatocarcinogenesis with underlying liver injury/fibrosis was assessed by a single dose of diethylnitrosamine (DEN) followed by repeated injections of CCl4. Genome-wide expression profiling was performed isolated stellate cells from these models to determine deregulated pathways. Results: Depletion of beta-PDGFR in hepatic stellate cells led to decreased histological liver injury, serum transaminases, collagen alpha 1(I) and alpha smooth muscle actin expression, and collagen deposition. Stellate cell proliferation was significantly reduced after acute hepatic injury in vivo. In contrast, autoactivation of beta-PDGFR in stellate cells accelerated liver fibrosis, most prominently after 6 weeks of CCl4 induced injury. There was no difference in development of DEN-induced pre-neoplastic loci according to the status of beta-PDGFR. Conclusions: Depletion of beta-PDGFR in hepatic stellate cells attenuated the development of liver injury, fibrosis, and stellate cell proliferation in multiple animal models, whereas the constitutive activation of beta-PDGFR enhanced fibrosis. However, manipulation of beta-PDGFR alone did not reduce development of dysplastic nodules. These findings indicate that titration of receptor beta-PDGFR expression on stellate cells parallels fibrosis and injury, but may not impact the development of hepatic neoplasia alone. Hepatic stellate cells were isolated from liver of beta-PDGFR-wild-type or knockout mice, and treated with beta-PDGF ligand or vehicle control.
2015-02-19 | E-GEOD-52253 | biostudies-arrayexpress
Project description:Deactivation of Hepatic Stellate Cells during Liver Fibrosis Resolution in Mice
| PRJNA168305 | ENA
Project description:Sex differences in liver gene expression are dictated by sex-differences in circulating growth hormone (GH) profiles. Presently, the pituitary hormone dependence of mouse liver gene expression was investigated on a global scale to discover sex-specific early GH response genes that might contribute to sex-specific regulation of downstream GH targets and to ascertain whether intrinsic sex-differences characterize hepatic responses to plasma GH stimulation. RNA expression analysis using 41,000-feature microarrays revealed two distinct classes of sex-specific mouse liver genes: genes subject to positive regulation (class-I) and genes subject to negative regulation by pituitary hormones (class-II). Genes activated or repressed in hypophysectomized (Hypox) mouse liver within 30-90min of GH pulse treatment at a physiological dose were identified as direct targets of GH action (early response genes). Intrinsic sex-differences in the GH responsiveness of a subset of these early response genes were observed. Notably, 45 male-specific genes, including five encoding transcriptional regulators that may mediate downstream sex-specific transcriptional responses, were rapidly induced by GH (within 30min) in Hypox male but not Hypox female mouse liver. The early GH response genes were enriched in 29 male-specific targets of the transcription factor Mef2, whose activation in hepatic stellate cells is associated with liver fibrosis leading to hepatocellular carcinoma, a male-predominant disease. Thus, the rapid activation by GH pulses of certain sex-specific genes is modulated by intrinsic sex-specific factors, which may be associated with prior hormone exposure (epigenetic mechanisms) or genetic factors that are pituitary-independent, and could contribute to sex-differences in predisposition to liver cancer or other hepatic pathophysiologies.
2010-01-27 | GSE17644 | GEO
Project description:Expression data from murine hepatic stellate cells
| PRJNA297410 | ENA
Project description:Analysis of hepatic stellate cells (HSCs) isoltaed from ASMA-HAS2 transgenic and HSC-specific Has2 knockout mice. HAS2 synthesized hyaluronic acid, one of major extracellular matrix. Results provide insight into the role of HAS2 in hepatic stellate cells.
2020-01-01 | GSE108593 | GEO
Project description:m6A-RIP sequencing of primary hepatic stellate cells (HSCs) isolated from Control and HSC-specific Mettl3-knockout (Mettl3 cKO) mouse liver tissues.
2022-07-13 | GSE207908 | GEO
Project description:Background. Abcb4 (-/-) mice secrete phosphatidylcholine-deficient bile and develop sclerosing cholangitis (SC). The cholangitis involves differential hepatic transcription of genes whose products govern inflammation, activation of hepatic stellate cells and fibrosis. This study was undertaken to test the hypothesis that several genes involved in regulation of tissue inflammation and fibrosis display transcription rates that reflect SC disease activity. Methods. Abcb4 (-/-) mice fed cholic acid (CA) display high SC activity and ursodeoxycholic acid (UDCA) fed mice display low SC activity. Differential hepatic transcription of genes was accordingly measured in abcb4 (-/-) mice maintained on CA- and UDCA-supplemented diets using cDNA microarrays. Abcb4 (+/+) mice served as controls. The differential transcription of selected genes was verified by real time polymerase chain reaction. Liver tissue pathology was quantified by histopathology scoring and immunohistochemistry to visualize bile duct cells and activated hepatic stellate cells. Results. Differential transcription of Ccl2, Ccl20, Cxcl10, Nfκb1, Nfκb2, Tgfβ1, Tgfβ2, Sparc, Ctgf, Lgals3, Elf3, Spp1, Pdgfa, Pdgfrb, Col1a1, Col1a2 and Col4a1 genes paralleled the differing SC activities of cholic acid- and UDCA-fed abcb4 (-/-) mice. Histopathology scores and immunohistochemistry showed greatly enhanced activation of hepatic stellate cells during high SC activity due to CA feeding. Conclusion. Differential transcription of several genes relating to tissue inflammation and hepatic stellate cell activation parallels SC activity in abcb4 (-/-) mice. Data on their differential transcription may be used to gauge SC disease activity.
2008-08-20 | GSE11507 | GEO
Project description:Aggf1 regulates the activation of hepatic stellate cells
| PRJNA303964 | ENA