Integrated analysis of hepatic miRNA and mRNA expression profiles in the spontaneous recovery of liver fibrosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA727615 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14340284.fastq.gz | Fastqsanger.gz | |||
| SRR14340285.fastq.gz | Fastqsanger.gz | |||
| SRR14340286.fastq.gz | Fastqsanger.gz | |||
| SRR14340287.fastq.gz | Fastqsanger.gz | |||
| SRR14340288.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 27 |
Similar Datasets
Project description:Liver fibrosis, results from the imbalance between extracellular matrix (ECM) production and degradation, is a common pathological consequence of various chronic liver diseases. Although a large number of miRNAs have been reported in liver fibrosis progression, miRNA-mRNA interactions involved in its reversal process remain to be fully elucidated. In the current study, we performed an integrated analysis of miRNA and mRNA expression profiles in a hepatic fibrosis recovery mouse model induced by thioacetamide. A total of 102 miRNA and 2,845 mRNAs showed significant differential expression in recovery mice compared to fibrotic mice. Moreover, 3,769 putative negatively correlated miRNA-mRNA pairs were revealed to be potentially implicated in the biological function regulation of small molecule metabolism and ECM organization. By integrating miRNA-mRNA regulatory networks, mmu-miR-1843a-5p, mmu-miR-193a-5p, mmu-miR-194-2-3p and mmu-miR-30c-2-3p were identified as lysyl oxidase-specific miRNAs that were associated with the pathogenesis of fibrosis recovery. Our results provide potential novel biomarkers and candidate targets for the treatment of liver fibrosis.
2022-04-26 | GSE173456 | GEO
Project description:Liver fibrosis, results from the imbalance between extracellular matrix (ECM) production and degradation, is a common pathological consequence of various chronic liver diseases. Although a large number of miRNAs have been reported in liver fibrosis progression, miRNA-mRNA interactions involved in its reversal process remain to be fully elucidated. In the current study, we performed an integrated analysis of miRNA and mRNA expression profiles in a hepatic fibrosis recovery mouse model induced by thioacetamide. A total of 102 miRNA and 2,845 mRNAs showed significant differential expression in recovery mice compared to fibrotic mice. Moreover, 3,769 putative negatively correlated miRNA-mRNA pairs were revealed to be potentially implicated in the biological function regulation of small molecule metabolism and ECM organization. By integrating miRNA-mRNA regulatory networks, mmu-miR-1843a-5p, mmu-miR-193a-5p, mmu-miR-194-2-3p and mmu-miR-30c-2-3p were identified as lysyl oxidase-specific miRNAs that were associated with the pathogenesis of fibrosis recovery. Our results provide potential novel biomarkers and candidate targets for the treatment of liver fibrosis.
2022-04-26 | GSE173961 | GEO
Project description:Integrated analysis of hepatic miRNA and mRNA expression profiles in the spontaneous recovery of liver fibrosis [miRNA]
| PRJNA725966 | ENA
Project description:Integrated analysis of hepatic miRNA and mRNA expression profiles in the spontaneous recovery of liver fibrosis [mRNA]
| PRJNA727618 | ENA
Project description:Nonalcoholic steatohepatitis (NASH) causes liver extracellular matrix (ECM) remodeling and is a risk factor for fibrosis and hepatocellular carcinoma (HCC). Microcystin-LR (MCLR) is a hepatotoxin produced by fresh-water cyanobacteria that causes a NASH-like phenotype, liver fibrosis, and is also a risk factor for HCC. The focus of the current study was to investigate and compare hepatic recovery after cessation of MCLR exposure in healthy versus NASH animals. Male Sprague-Dawley rats were fed either a control or a high fat/high cholesterol (HFHC) diet for eight weeks. Animals received either vehicle or 30 µg/kg MCLR (i.p: 2 weeks, alternate days). Animals were euthanized at one of three time points: at the completion of the MCLR exposure period and after 2 and 4 weeks of recovery. Histological staining suggested that after four weeks of recovery the MCLR-exposed HFHC group had less steatosis and more fibrosis compared to the vehicle-exposed HFHC group and MCLR-exposed control group. RNA-Seq analysis revealed dysregulation of ECM genes after MCLR exposure in both control and HFHC groups that persisted only in the HFHC groups during recovery. After 4 weeks of recovery, MCLR hepatotoxicity in pre-existing NASH persistently dysregulated genes related to cellular differentiation and HCC. These data demonstrate impaired hepatic recovery and persistent carcinogenic changes after MCLR toxicity in pre-existing NASH.
2021-11-06 | GSE188231 | GEO
Project description:In schistosomiasis japonica, the egg-induced granulomatous response and the development of extensive hepatic fibrosis is the main pathology. Information regarding the specific mechanisms associated with granuloma regression and the subsequent recovery events in the host liver are still limited. In this study, a murine model of schistosomiasis japonica was used to characterise the multicellular pathways occurring during liver regeneration. Schistosoma japonicum-infected C57BL/6 mice were administered with the drug praziquantel (PZQ), on a daily basis for five consecutive days to eliminate all adult parasites. The pathological changes of PZQ-treated groups after 3, 6 and 7 weeks post PZQ treatment were examined, along with the assessment of cellular infiltration to the liver. PZQ treatment significantly reduced the degree of splenomegaly, granuloma density and the collagen deposition of liver fibrosis. The infiltration of inflammatory cells, including neutrophils, eosinophils and macrophages to the liver were as well significantly decreased. Transcriptomic analysis revealed the significant up-regulation of fatty acid metabolism genes and the identification of peroxisome proliferator-activated receptor alpha (PPAR-α) as the upstream regulator during the process of liver recovery. Aryl hydrocarbon receptor (AhR) signalling pathway that is involved primarily in the regulation of hepatic enzymes responsible for xenobiotic metabolism was as well differentially up-regulated. These findings indicate that schistosome egg-induced fibrogenesis process is reversible, and provide a better understanding of the regression mechanisms associated with hepatic schistosomiasis. These results hold important implications for the future alleviation of this and other fibrotic diseases of clinical significance. C57BL/6 murine model infected with S. japonicum were treated orally with Praziquantel (PZQ) after 7 weeks post infection to examine the hepatic regression process following drug treatment. These PZQ-treated, non PZQ-treated and uninfected mice were then euthanised at 10, 13, and 14 weeks p.i. Livers were collected from each mice, and subjected to total RNA isolation and gene expression analysis. Microarray analysis of this study was performed using samples derived from 3 individual mice per group/time-point.
2014-08-31 | E-GEOD-59276 | biostudies-arrayexpress
Project description:A differential label-fee proteomics approach was performed using 27 biopsies from patients with HCV-associated hepatic fibrosis. For statistical analysis the patients were grouped into a low and a high fibrosis group. The low fibrosis group contained 13 patients of fibrosis stages 0, 1 and 2, whereas the high fibrosis group contained 14 patients of fibrosis stages 3 and 4 (fibrosis stages according to Batts-Ludwig classification).
2015-03-30 | PXD001474 | Pride
Project description:Aim: Hepatic fibrosis is a major worldwide medical problem and can develop into liver cirrhosis and hepatocellular carcinoma(HCC). Until now, there are no effective drugs for liver ?brosis because the molecular mechanism of progression of liver fibrosis is not fully understood. MicroRNAs (miRNAs) are an important class of small non-coding functional RNAs that play a key role in many biological processes. The purpose of this study was to clarify how the aberrant expression of miRNAs participates in development of the liver fibrosis in rat liver fibrosis model. Methods: Fibrotic and paired normal liver tissues were collected and assesssed by deep sequencing technology. MiRNA pro?ling results were validated by quantitative real-time polymerase chain reaction (qRT-PCR) and bioinformatics was used to predict miRNA targets. Results: Nine deregulated miRNAs were induced in porcine serum (PS)-induced hepatic fibrosis versus normal liver. Further analysis revealed several signaling pathways (e.g., gap junction and neuroactive ligand-receptor interaction) may be associated with hepatic fibrogenesis. Conclusion: Several miRNAs are dysregulated in PS-induced hepatic fibrosis and seem to be closely associated with hepatic fibrogenesis. These results provide an experimental basis for understanding the mechanism of hepatic fibrosis. We sequenced two samples, including case and control. Each sample has two replicates.
2015-06-04 | E-GEOD-54028 | biostudies-arrayexpress
Project description:<p>Hepatic fibrosis decreased feces bile acid level. Hepatic fibrosis increased serum bile acid. This result showed that hepatic fibrosis inhibited the excretion of bile acid in clinical patients. This result provided phenotype for hepatic fibrosis patients. Bile acid was important indexes for liver injury. TCDCA was important, and it play toxicity effect through ferroptosis and apoptosis. The research for other bile acid such CA, UDCA, TUDCA, TDCA, LCA, TLCA would be important.</p><p><br></p><p><strong>Hepatic fibrosis serum (sample 1) analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'><strong>MTBLS6732</strong></a>.</p><p><strong>Hepatic fibrosis feces (sample 2) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'><strong>MTBLS6742</strong></a>.</p><p><strong>Hepatic fibrosis serum+feces (sample 3) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'><strong>MTBLS6728</strong></a>.</p>
2023-03-17 | MTBLS6732 | MetaboLights
Project description:<p>Hepatic fibrosis decreased feces bile acid level. Hepatic fibrosis increased serum bile acid. This result showed that hepatic fibrosis inhibited the excretion of bile acid in clinical patients. This result provided phenotype for hepatic fibrosis patients. Bile acid was important indexes for liver injury. TCDCA was important, and it play toxicity effect through ferroptosis and apoptosis. The research for other bile acid such CA, UDCA, TUDCA, TDCA, LCA, TLCA would be important.</p><p><br></p><p><strong>Hepatic fibrosis feces (sample 2) analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'><strong>MTBLS6742</strong></a>.</p><p><strong>Hepatic fibrosis serum (sample 1) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'><strong>MTBLS6732</strong></a>.</p><p><strong>Hepatic fibrosis serum+feces (sample 3) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'><strong>MTBLS6728</strong></a>.</p>
2023-03-17 | MTBLS6742 | MetaboLights