Liver fibrosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA857444 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20073700.fastq.gz | Fastqsanger.gz | |||
| SRR20073701.fastq.gz | Fastqsanger.gz | |||
| SRR20073702.fastq.gz | Fastqsanger.gz | |||
| SRR20073703.fastq.gz | Fastqsanger.gz | |||
| SRR20073704.fastq.gz | Fastqsanger.gz |
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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
Project description:The aim of this study is to compare mild and advanced liver fibrosis gene expression profiling and to identify novel markers of fibrosis progression. By transcriptome analysis with a cDNA array virtually covering every transcript in liver, we compared transcript levels in mild (F1 Metavir score) and advanced (F4 Metavir score) fibrosis. A stringent selection identified a list of 16 transcripts which completely separated the 2 groups of patients (8 F1 and 8 F4). We report that dysregulations at the transcriptional level do exist between mild fibrosis (F1) and advanced fibrosis (F4). Keywords: fibrosis stage-dependent analysis Fibrosis samples were analyzed for 16 patients : 8 mild fibrosis (F1-1 to F1-8) and 8 advanced fibrosis (F4-1 to F4-8). All data in the current study were obtained from 3 separate hybridizations per RNA sample.
2008-05-24 | E-GEOD-11536 | biostudies-arrayexpress
Project description:Background/Aim: We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods: This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Methods: This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results: NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion: Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease.
2021-07-15 | GSE179961 | GEO
Project description:Transcriptional dynamics of hepatic stellate cells in experimental acute liver injury, liver fibrosis and liver fibrosis reversal.
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Project description:The aim of this study is to compare mild and advanced liver fibrosis gene expression profiling and to identify novel markers of fibrosis progression. By transcriptome analysis with a cDNA array virtually covering every transcript in liver, we compared transcript levels in mild (F1 Metavir score) and advanced (F4 Metavir score) fibrosis. A stringent selection identified a list of 16 transcripts which completely separated the 2 groups of patients (8 F1 and 8 F4). We report that dysregulations at the transcriptional level do exist between mild fibrosis (F1) and advanced fibrosis (F4). Keywords: fibrosis stage-dependent analysis
2008-05-24 | GSE11536 | GEO
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.
2015-03-31 | GSE67423 | GEO
Project description:Establish the miRNA expression profile between advanced liver fibrosis and liver without fibrosis in mice
2011-01-12 | GSE19865 | GEO
Project description:To investigate the differential gene expression of m6A RNA methylation in cholestatic liver fibrosis, we extablished a mouse model of liver fibrosis by common bile duct ligation.
2024-12-31 | GSE218407 | GEO
Project description:Liver fibrosis is an urgent clinical problem without effective treatment. Herein, we conducted a high-content screening on a natural “privileged” diterpenoid library to identify a potent anti-liver fibrosis lead DP. Leveraging photoaffinity labeling approach, apolipoprotein L2 (APOL2), an ER-rich protein, was identified as the direct target of DP. APOL2 is mainly expressed in activated hepatic stellate cells (HSCs) and could activate HSCs to synthesize ECM proteins. It can be induced by TGF-β1 and be antagonized by DP. Mechanistically, upon TGF-β1stimulation, APOL2 binds ER Ca2+ pump SERCA2 to trigger ER stress, elevating its downstream PERK-HES1 axis to promote liver fibrosis, mildly dependent on the canonical TGF-β/Smad signaling. As a result, ablation of APOL2 significantly alleviated TGF-β1-stimulated HSCs activation, and abolished anti-fibrosis effect of DP. Our findings not only define APOL2 as a novel therapeutic target for liver fibrosis, but also highlight DP as a promising lead for treatment of this symptom.
2024-08-13 | PXD047924 | Pride
Project description:Carbon tetrachloride (CCl4) induced liver fibrosis
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