Genomics data for CCl4-induced mice liver fibrosis
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ABSTRACT:
PROVIDER: PRJNA1158696 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30599631_1.fastq.gz | Fastqsanger.gz | |||
| SRR30599631_2.fastq.gz | Fastqsanger.gz | |||
| SRR30599632_1.fastq.gz | Fastqsanger.gz | |||
| SRR30599632_2.fastq.gz | Fastqsanger.gz | |||
| SRR30599633_1.fastq.gz | Fastqsanger.gz |
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Project description:Objective: To understand the transcriptome data of liver fibrosis induced by CCl4 in mice.Methods: C57BL/6 mice were used to duplicate the liver fibrosis model induced by CCl-4.After successful replication, mouse RNA was extracted for subsequent experiments.The basic principle of RNA extraction is to prevent RNA degradation during extraction, maximize RNA extraction efficiency, and ensure the extraction of high-quality RNA with good integrity and purity from target samples.According to the species (such as animal sample or plant sample) and sample status (such as animal tissue or animal cell) of the sample, select the appropriate extraction reagent and corresponding extraction method.The detection of high-quality RNA in samples is the basis for the success of the whole project. In order to ensure the accuracy of sequencing data, we performed quality inspection on samples, and the library construction can only be performed after the detection results meet the requirements for sequencing library construction.Sample test results are shown in the quality inspection report.After the library construction samples passed the test, the mRNA of eukaryotes was enriched with magnetic beads with Oligo (dT).Subsequently fragmentation buffer was added to randomly interrupt the mRNA.First-strand cDNA was synthesized using mRNA as a template with a six-base random primer (random hexamers), followed by buffer, dNTPs, and DNA polymerase I to synthesize the second-strand cDNA, which was subsequently purified using AMPure XP beads.Purified double-stranded cDNA was then end-repaired, A-tailed and ligated with sequencing adapters, followed by fragment size selection with AMPure XP beads, and finally PCR enrichment to obtain the final cDNA library.After library construction, insert size and effective concentration of the library were tested to ensure library quality.After passing the library test, different libraries were pooling according to the amount of data under the target and sequenced on the machine.RESULTS: RNA-seq data of CCL4-induced liver fibrosis model in mice were finally obtained in our experiment, which provided a molecular biological basis for our future study of liver fibrosis in mice.
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Project description:To understand the fibrotic response in the CCl4 induced liver fibrosis model, we performed RNA-seq of liver samples from mice treated with oil or CCl4.
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Project description:Carbon tetrachloride (CCl4) induced liver fibrosis
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Project description:This study aimed to investigate the protective mechanisms of helenalin on hepatic fibrosis,Rats were intragastrically administrated with 50% CCl4 for 9 weeks to induce liver fibrosis, followed by various medicines for 6 weeks. The transcriptomic analysis was performed in liver tissues by RNA-seq.
2021-11-25 | GSE189402 | GEO
Project description:To investigate the differences in microRNA expression profiles between fibrotic and normal livers, we performed microRNA microarrays for total RNA extracts isolated from mouse livers treated with carbontetrachloride (CCl4) or corn-oil for 10 weeks (n=3/group). MicroRNAs were considered to have significant differences in expression level when the expression difference showed more than two-fold change between the experimental and control groups at p<0.05. We found that 12 miRNAs were differentially expressed in CCl4-induced fibrotic liver. To induce chronic liver fibrosis, seven-week-old mice received 0.6 ml/kg body weight of carbon-tetrachloride (CCl4) dissolved in corn-oil by intraperitoneal (i.p.) injection, twice a week for 10 weeks (n=3). As a control, same number of mice was injected with equal volume of corn-oil for 10 weeks.
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Project description:Liver fibrosis is a multifactorial trait that develops in response to chronic liver injury. Our aim was to characterize the genetic architecture of carbon tetrachloride (CCl4)-induced liver fibrosis using the Hybrid Mouse Diversity Panel (HMDP), a panel of over 100 genetically distinct mouse strains optimized for genome wide association studies and systems genetics. Chronic liver injury was induced by CCl4 injections twice weekly for six weeks. 437 mice received CCl4 and 256 received vehicle, after which animals were sacrificed for liver histology and gene expression. Using automated digital image analysis, we quantified fibrosis as the collagen proportionate area % (CPA%) of the whole section, excluding normal collagen. We discovered broad variation in fibrosis among the HMDP strains, demonstrating a significant genetic influence on this trait, with an estimated heritability (H2) of 44%. Genome-wide association analyses revealed significant and suggestive loci underlying susceptibility to fibrosis, some of which overlapped with loci identified in mouse crosses and human population studies. Liver global gene expression was assessed by RNA sequencing, and gene set enrichment analyses identified the underlying pathways, of which stellate cell involvement was prominent. We also performed expression quantitative trait locus analyses to identify strong causal candidate genes. Our results provide a rich resource for the design of experiments to understand mechanisms underlying fibrosis and for rational strain selection when testing anti-fibrotic drugs.
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Project description:Long non-coding RNAs (lncRNAs) are involved in numerous biological functions and pathological processes. In this study, we have identified a novel lncRNA ENSMUST00000147617, named Highly Expressed in Liver Fibrosis (lnc-HELF), which is remarkably up-regulated in mouse and human fibrotic livers. To identify the roles of lnc-HELF in liver fibrosis, we performed RNA-seq to analyze the effect of lnc-HELF deficient on CCl4-induced liver fibrosis. The mice were divided in three groups: mice treated with CCl4 in combination with injection of AAV8-NC (NC_CCl4, n=3), mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF1# (sh1_CCl4, n=3) and mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF2# (sh2_CCl4, n=3).
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Project description:This study is aimed to investigate the underlying mechanisms of didymin on anti-hepatic fibrosis. In brief, mice were randomly devided into three groups,including normal, CCl4 and didymin groups. Except the normal group, mice were intra-peritonelly administrated with 20% CCl4 for 10 weeks to induce liver fibrosis; after modeling successfully, mice in didymin group were subsequently intragastrically administrated with didymin for 6 weeks. Finally, the transcriptomic analysis was performed to acquire the differently expressed genes amog the three groups, trying to figure out the potential targets, which regulated by didymin.
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Project description:Transcriptional Profiling of liver fibrosis induced by CCl4 injections
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Project description:Transcriptomic profile of liver fibrosis in mice induced by CCl4
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