Gene Expression Analysis of Fibrotic Liver
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE55747 | GEO | 2017/03/06
SECONDARY ACCESSION(S): PRJNA240887
REPOSITORIES: GEO
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Project description:The aim of this study was to investigate FSP1 in human and experimental liver disease, and to characterize FSP1-positive cells. Results: FSP1-positive cells are increased in human and experimental liver diseases including liver cancer but do not synthesize type I collagen or express other classical markers of myofibroblasts including aSMA and desmin. Surprisingly, FSP1 positive cells express F4/80 and other markers characteristic of the myeloid-monocytic lineage as evaluated by double-immunofluorescence staining, cell fate tracking, flow cytometry andtranscriptional profiling. Conclusion: These findings suggest that FSP1 is a marker of a subset of macrophages in liver injury, fibrosis and cancer.
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Project description:The aim of this study was to investigate FSP1 in human and experimental liver disease, and to characterize FSP1-positive cells. Results: FSP1-positive cells are increased in human and experimental liver diseases including liver cancer but do not synthesize type I collagen or express other classical markers of myofibroblasts including aSMA and desmin. Surprisingly, FSP1 positive cells express F4/80 and other markers characteristic of the myeloid-monocytic lineage as evaluated by double-immunofluorescence staining, cell fate tracking, flow cytometry andtranscriptional profiling. Conclusion: These findings suggest that FSP1 is a marker of a subset of macrophages in liver injury, fibrosis and cancer.
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Project description:Long noncoding RNAs (lncRNAs) play important roles in various biological processes; however, few have been identified that regulate hepatic stellate cells (HSCs) activation and the progression of liver fibrosis. To identify the possible roles of lncRNAs in regulating liver fiboris and the potential of lncRNAs as molecular markers for liver fiboris, we systematically analyzed the regulation of lncRNAs and mRNAs in a mouse model of carbon tetrachloride (CCl4)-induced liver fibrogenesis by microarray analysis, which revealed a panel of lncRNAs and mRNAs that were specifically regulated in livers of mice undergoing hepatic fibrosis. To identify the possible roles of lncRNAs in regulating liver fiboris and the potential of lncRNAs as molecular markers for liver fiboris,we determined the lncRNA and mRNA expression profiles in the livers of fibrotic mice and normal mice by lncRNA and mRNA microarrays.
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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.
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Project description:RNA sequencing was performed on uninjured, and injured (FSP1, and aSMA expressing) fibroblasts from mice hearts. Fibrosis accompanying wound healing can drive the failure of many different organs. Activated fibroblasts are the principal determinants of post-injury pathological fibrosis as well as physiological repair, making them a difficult therapeutic target. Fibroblasts are a heterogeneous cell population lacking unique functional classification. We demonstrated that FSP1 and αSMA expressing cells are distinct, post-injury fibroblasts in the heart, kidney, and skin and exhibit unique temporal expression patterns. Using mice that express GFP under the FSP1 or αSMA promoters, we isolated these fibroblasts from mouse hearts after myocardial infarction. Protein and transcript arrays, cellular assays as well as in vivo granulation tissue formation were used to determine their functional role(s) in healing and fibrosis. Whereas αSMA+ fibroblasts predominated in producing matrix proteins, FSP1+ fibroblasts significantly promoted angiogenesis. These studies have the potential to shift our focus towards viewing fibroblasts not only molecularly but also as functionally heterogeneous and provide a new paradigm with which to approach treatment for organ fibrosis.
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Project description:loss of Hmgb2 in vivo in mouse liver largely prevented CCl4-induced liver fibrosis. The goal of the RNA-seq is to identify the Hmgb2 regulated genes in CCL4 induced liver fibrosis.
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Project description:Carbon tetrachloride (CCl4) induced liver fibrosis
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