Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1024692 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26328219_1.fastq.gz | Fastqsanger.gz | |||
| SRR26328219_2.fastq.gz | Fastqsanger.gz | |||
| SRR26328220_1.fastq.gz | Fastqsanger.gz | |||
| SRR26328220_2.fastq.gz | Fastqsanger.gz | |||
| SRR26328221_1.fastq.gz | Fastqsanger.gz |
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Project description:Liver fibrosis has been implicated in the pathogenesis of various liver disease. Thus far, there is still no effective intervention means for this process. Recently, we have demonstrated that S100A16 participated in liver lipid accumulation and renal fibrosis. Therefore, we hypothesized that S100A16 took a critical role in liver fibrosis. S100a16 transgenic and knockdown mice were generated and stimulated with carbon tetrachloride, bile duct ligation and methionine choline deficiency diet. Alterations of gene expression in hepatic stellate cells from wild type and S100a16+/- mice were investigated by transcriptome sequencing. S100A16 expression levels in liver tissue of patients and rodent models of liver fibrosis were markedly increased. S100a16 transgenic mice showed spontaneous liver fibrosis after normal feeding for 6 months. On the contrary, silencing of S100a16 exhibited obvious protective effect against liver fibrosis caused by different stimulations. Meanwhile, results showed that deletion of S100a16 significantly inhibited hepatic stellate cells (HSCs) activation cultured in fetal bovine serum contained medium. RNA sequencing results revealed that mechanistically, C-X-C motif chemokine receptor 4 (Cxcr4) participated in the process of S100a16 in liver fibrosis. Knockdown of S100a16 inhibited Cxcr4 expression through augmenting P53 expression. SDF-1α/CXCR4-dependent extracellular signal-regulated kinase 1/2 and Akt phosphorylation mediated the effects of S100a16 on α-smooth muscle actin expression and HSCs activation. These data indicate that S100a16 deficiency prevents liver fibrosis by inhibiting Cxcr4 expression. Targeting S100A16 may provide insights into the pathogenesis of liver fibrosis and pave the way for developing strategies for liver fibrosis-related diseases prevention and treatment.
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Project description:Although treatment of chronic hepatitis C virus (HCV) infection with direct acting antivirals (DAAs) results in high rates of cure, liver fibrosis does not resolve immediately after HCV eradication. Resolution of fibrosis occurs in some, but not all patients, after HCV cure, and hepatic decompensation and hepatocellular carcinoma can still occur in patients with pre-existing cirrhosis. We hypothesized that evaluation of the host liver proteome in the context of HCV treatment would provide insight into how inflammatory and fibrinogenic pathways change upon HCV eradication. We evaluated the whole liver proteome and phosphoproteome using paired liver biopsies from 8 HCV-infected patients collected before or immediately after treatment with DAAs in clinical trials. We identify interferon stimulated proteins as the predominant pathways that decrease with HCV treatment, which is consistent with previous analyses of the liver transcriptome during DAA therapy. While there was no change in the proteome of pathways associated with liver fibrosis, we identified a decrease in the phosphoproteome signature for ERK1/ERK2 as a result of HCV treatment. Conclusion: There is a reduction in the endogenous interferon-mediated antiviral response and alterations in the phosphoproteome that may precede resolution of fibrosis in the liver immediately after treatment of HCV with DAAs.
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