Transcriptional dynamics of hepatic stellate cells during first hours of in vitro activation
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ABSTRACT:
PROVIDER: PRJNA727548 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14432324.fastq.gz | Fastqsanger.gz | |||
| SRR14432325.fastq.gz | Fastqsanger.gz | |||
| SRR14432326.fastq.gz | Fastqsanger.gz | |||
| SRR14432327.fastq.gz | Fastqsanger.gz | |||
| SRR14432328.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Gene expression of mouse hepatic stellate cells was characterized under the following conditions: Quiescent (isolated from normal mouse liver) and reverted (isolated from mouse liver treated with 4 injections of carbontetrachloride followed by 45 day rest period) Affymetrix Mouse 1.0ST gene expression measurements were used to characterize the transcriptomic basis in quiescent hepatic stellate cells, isolated from normal liver, and reverted hepatic stellate cells, isolated from liver treated with 4 injections of CCl4 followed by a 45 day rest period. Gene expression of mouse hepatic stellate cells was characterized under the following conditions: A. Quiescent control hepatic stellate cells (n=4). B. Reverted hepatic stellate cells (n=4).
2014-05-05 | E-GEOD-38648 | biostudies-arrayexpress
Project description:Hepatic stellate cell autophagy inhibits extracellular vesicle release to attenuate liver fibrosis. Primary human hepatic stellate cells were treated with PDGF or PDGF + SHP2 inhibitor. RNA was purified and submitted for sequencing to Mayo Clinic Genomics Core. After applying the filters FDR>0.05, Log2(FC)>1 and RPKM>15, we ended up with nearly 300 genes differentially regulated between the two conditions. Ingenuity Pathway Analysis revealed that Ostheoarthritis was the first pathway to be differentially regulated. From this pathway, REDD1 (DDIT4 transcript), an mTOR inhibitor, was further explored, especially in the context of extracellular vesicle release.
2019-11-08 | GSE140110 | GEO
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:Analysis of hepatic stellate cells isoltaed from wild-type, TLR4-/-, and CD44-/- mice. TLR4 and CD44 are major hyaluronic acid receptors. Results provide insight into the effects of TLR4 and CD44 loss in hepatic stellate cells.
2020-01-01 | GSE109200 | GEO
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:Located in the perisinusoidal space of Disse, hepatic stellate cells (HSCs) communicate with all other liver cell types by physical association and / or by producing cytokines and chemokines. In liver disease and folllowing liver transplantation, elevated levels of endotoxin (bacterial lipopolysaccharide: LPS) stimulate HSCs to produce increased amounts of cytokines and chemokines. Transcriptomic analysis of cultured HSCs stimulated with LPS yields a survey of expression changes which potentially modulate the hepatic inflammatory and immune responses. In two independent experiments, rat HSCs were cultured with or without 10 ng/ml LPS for 1h and 24h, then harvested for microarray analysis (i.e., 8 samples). In the first of these experiments, cells also were also harvested after 3, 6 and 12 hours of LPS treatment, for a total of 11 samples.
2013-10-31 | E-GEOD-49980 | biostudies-arrayexpress
Project description:Purpose: The goal of this study was to determine biological consequences during liver regeneration following partial hepatectomy in mice by next-generation sequencing. A particular interest was to compare mice with either a floxed b-PDGFR allele to mice that harbored a deletion of b-PDGFR in hepatic stellate cells (HSCs), by crossing b-PDGFR fl/fl mice with transgenic GFAP-Cre mice. Methods: b-PDGFR fl/fl mice or mice with a HSC-specific deletion of b-PDGFR underwent either sham operation or 70% partial hepatectomy. Following 72 hours, livers were collected and total RNA was extracted using tizol, followed by a purification using Quiagen spin columns including an on-column DNAse digestion step. Conclusion: Our study represents a detailed analysis of hepatic transcriptome, with biologic replicates, generated by RNA-seq technology of livers following sham operation or partial hepatectomy in b-PDGFR fl/fl mice or b-PDGFRfl/fl/GRAP-Cre mice. Whole liver mRNA profiles of sham operated livers or livers collected 72hours after partial hepatectomy of beta-PDGFR fl/fl and beta-PDGFR fl/fl/GFAP-Cre (creating a hepatic stellate cell-specific deletion of b-PDGFR) mice were generated by deep sequencing, in duplicate, using Illumina HiSeq2000.
2013-11-08 | E-GEOD-52234 | biostudies-arrayexpress
Project description:Hepatic Stellate Cell Activation after 72hr
| PRJNA948023 | ENA