Hepatic Stellate Cell Activation after 72hr
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ABSTRACT:
PROVIDER: PRJNA948023 | ENA |
REPOSITORIES: ENA
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Project description:Early during culture of primary mouse HSCs gene expression changes. These expression alterations can be affected by treating cells with histone deacetylase inhibitor, valproic acid Primary mouse Hepatic stellate cells were cultured for short periods of time (4-16-64h) in presence or absence of valproic acid. Gene expression analysis (mouse Gene 1.0 ST arrays according to manufacturerM-bM-^@M-^Ys manual 701880Rev4 (Affymetrix, Santa Clara, CA)), in vitro stellate cell activation and inhibition of the activation by valproic acid treatment.
2014-01-01 | E-GEOD-51882 | biostudies-arrayexpress
Project description:RNA-seq of Monocyte-derived Macrophages and Hepatic Stellate Cell Activation after 72hr
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Project description:To investigate the role of Tet2 deficient immune cells in hepatic stellate cell activation, wild type or Tet2 deficient B cells, T cells, and hepatic macrophages were isolated and co-cultured with purified hepatic stellate cells. Gene expression profiling analysis of bulk hepatic stellate cell RNA was then performed.
2023-02-07 | GSE223693 | GEO
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
Project description:Transcriptional alterations during the first hours of hepatic stellate cell activation were determined using RNA Sequencing. Cultured hepatic stellate cells were collected for RNA Sequencing at several timepoints during the first 24 hours. Illumina NovaSeq SP was used for sequencing.
2021-12-15 | GSE173920 | GEO
Project description:Analysis of human hepatic stellate cell line LX2 stimulated for 24h in serum-free DMEM medium containing 0 or 50 ng/ml recombinant human GDF2 protein. Results provide insight into the activation effects of GDF2 on human hepatic stellate cell. We used microarrays to detail the global programme of gene expression underlying activation of hepatic stellate cells and identified liver-fibrosis-related genes genes during this process.
2019-09-05 | GSE104482 | GEO
Project description:Hepatic Stellate Cells activation induced by Lhx2 deletion
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Project description:Activation and migration of hepatic stellate cells (HSCs) followed by matrix deposition are characteristics of liver fibrosis. Several studies have shown the importance of hepatocyte and endothelial cell-derived extracellular vesicles (EVs) in liver pathobiology. However, less is known about the role of HSC-derived EVs in liver diseases. In this study, we investigated the molecules released through HSC-derived EVs and whether these can promote fibrosis.
2018-10-18 | PXD007258 | Pride
Project description:The Hippo pathway effector YAP controls mouse hepatic stellate cell activation
| PRJNA643776 | ENA
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