Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA282907 | ENA |
REPOSITORIES: ENA
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Project description:The molecular determinants of a healthy human liver cell phenotype remain largely uncharacterized. In addition, the gene expression changes associated with activation of primary human hepatic stellate cells, a key event during fibrogenesis, remain poorly characterized. Here, we provide the transriptomic profile underpinning the healthy phenotype of human hepatocytes, liver sinusoidal endothelial cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as activated HSCs (aHSCs) We assess the transcriptome for purified, non-cultured human hepatocytes, liver sinusoidal cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as culture-activated HSCs (aHSCs).
2016-03-02 | GSE68000 | GEO
Project description:The molecular determinants of a healthy human liver cell phenotype remain largely uncharacterized. In addition, the gene expression changes associated with activation of primary human hepatic stellate cells, a key event during fibrogenesis, remain poorly characterized. Here, we provide the transriptomic profile underpinning the healthy phenotype of human hepatocytes, liver sinusoidal endothelial cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as activated HSCs (aHSCs) We assess the transcriptome for purified, non-cultured human hepatocytes, liver sinusoidal cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as culture-activated HSCs (aHSCs). Hepatocytes (n=2 donors), LSECs (n=3), qHSCs (n=3) and in vitro activated HSCs (n=3; from the same donors as the qHSCs and LSECs) were used for this study.
2016-03-02 | E-GEOD-68000 | biostudies-arrayexpress
Project description:Human hepatic stellate cell line LX-2 activated under acidic culture condition
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Project description:Adult-derived human liver stem/progenitor cells (ADHLSC) are obtained after primary culture of the liver parenchymal fraction. The cells are of fibroblastic morphology and exhibit a hepato-mesenchymal phenotype. Hepatic stellate cells (HSC) derived from the liver non-parenchymal fraction present a comparable morphology as ADHLSC. Because both ADHLSC and HSC are described as liver stem/progenitor cells, we strived to extensively compare both cell populations at different levels and to propose tools demonstrating their singularity. The database include full expression (HGU-219) measurements samples from 7 Adult-Derived Human Liver Stem/progenitor (n=7) and human hepatic stellate samples (n=7)
2015-05-11 | E-GEOD-49995 | biostudies-arrayexpress
Project description:Expression analysis of growing and senescent activated hepatic stellate cells
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Project description:We have established culture systems to generate liver sinusoidal endothelial cells (LSECs) and hepatic stellate cells (HSCs) from hiPSCs. To characterize gene expression profiling in hiPSC-derived LSECs and HSCs, transcriptome analysis was performed.
2017-07-27 | GSE92771 | GEO
Project description:Genome-wide analysis of DNA methylation and gene expression patterns in purified, uncultured human liver cells and activated hepatic stellate cells
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Project description:Activated hepatic stellate cells (HSC) that transdifferentiate to myofibroblasts in the injured liver are responsible for scar formation that leads to fibrosis and eventually cirrhosis. To investigate the gene expression profile during different stages of this process, we performed serial analysis of gene expression (SAGE), representing a quantitative and qualitative description of all expressed genes. Stellate cells were isolated from human livers and cultured. SAGE was performed on RNA isolated from quiescent, activated and transdifferentiated HSC. Comparison of the three resulting transcriptomes showed that less than 5% of all genes changed significantly in expression. Established markers of liver fibrosis showed enhanced expression in accordance with the transdifferentiation process. In addition, induction was seen for several genes not yet recognized to be involved in liver fibrosis, such as insulin-like growth factor binding proteins (IGFBP) and antagonists of bone morphogenic proteins: follistatin and gremlin. The induction of these genes was validated in vivo in mice developing liver fibrosis. The expression of IGFBPs and gremlin was measurable in the livers of these mice while it was low or undetectable in control mice without liver fibrosis. Since gremlin modulates the activity of bone morphogenic growth factors, it may represent a novel pathway and a target for therapeutic intervention and together with IGFBPs as a specific marker of liver fibrosis. In conclusion, the comparison of the three transcriptomes of (activated) stellate cells reveals novel genes involved in fibrogenesis and provides an appreciation of the sequence and timing of the fibrotic process in liver. Keywords: cell type comparison Human hepatic stellate cells (HSC) were isolated from wedge sections of normal human liver unsuitable for transplantation or from tumor-free human liver after partial hepatectomy as previously reported. Briefly, after a combined digestion with collagenase/pronase, HSC were separated from other liver nonparenchymal cells by ultracentrifugation over gradients of Larcoll (Sigma). The percentage of HSC in these isolates was > 90% as assessed by transmission microscopy, autofluorescence of vitamin A and immunofluorescence of vimentin. Immediately after isolation RNA was extracted for the construction of the SAGE library of quiescent HSC. To obtain activated stellate cells, these cells were cultured for 15 days on plastic culture dishes in modified Dulbecco's medium supplemented with 0.6 U/ml insulin, 2.0 mmol/L glutamine, 0.1 mmol/L nonessential amino acids, 1.0 mmol/L sodium pyruvate, antibiotic antifungal solution (Gibco) and 20% fetal bovine serum. To obtain fully transdifferentiated hepatic stellate cells, or myofibroblasts, the cells were cultured until they had reached passage 6 to 7. Myofibroblast phenotype was confirmed by detection of vimentin and ?-smooth muscle actin using immunofluorescence with monoclonal antibodies from Dako and Sigma, respectively. Medium was refreshed twice a week and at the indicated period RNA was extracted using Trizol (Quiagen)
2006-07-01 | E-GEOD-5022 | biostudies-arrayexpress
Project description:It is still unclear whether hepatic stellate cells (HSC) activate in a similar manner in different chronic liver disease aetiologies. Here, we investigate how human stellate cells activate in vitro at the transcriptome level.
2024-10-25 | GSE276915 | GEO
Project description:Hepatic stellate cells (HSCs) experience phenotypic transformation, from the quiescent phenotype to the activated one, after different etiologies of liver injury. Liver fibrosis is then occurred upon the activation of HSCs. miR-16 deficiency is identified to be an important characteristic of HSCs activation. We used Affymetrix rat 230 2.0 arrays (Affymetrix, Santa Clara, U.S.A.) to uncover the global alternations of transcriptome under miR-16 restoration. We isolated quiescent hepatic stellate cells (HSCs) from adult male SD rats (normal control group) by in situ perfusion and density-gradient centrifugation. Activated HSCs were separated from rats of fibrosis model group, which were treated by 40% carbon tetrachloride (CCl4) for 8 weeks, by means of liver section, digestion and sequential centrifugation. Quiescent and activated HSCs were then divided into 4 groups at random, namely quiescent HSCs, activated HSCs, pLV-miR-16-treated HSCs and pLV-GFP-treated HSCs. The pLV-miR-16-treated group, pLV-GFP-treated group were infected with pLV-miR-16 and pLV-GFP, respectively.
2012-08-28 | E-GEOD-40381 | biostudies-arrayexpress