Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1081628 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28130500_1.fastq.gz | Fastqsanger.gz | |||
| SRR28130500_2.fastq.gz | Fastqsanger.gz | |||
| SRR28130501_1.fastq.gz | Fastqsanger.gz | |||
| SRR28130501_2.fastq.gz | Fastqsanger.gz | |||
| SRR28130502_1.fastq.gz | Fastqsanger.gz |
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Project description:HBV-transgenic mice were treated i.v. with 1x10e11 particles AAV serotype 8 vectors expressing different RNAi-triggers targeting the HBV transcripts. To determine possible toxicities caused by the different vectors (including off-target activity against endogenous genes) we performed a whole transcriptome analysis of RNA of livers harvested 15 days after injection.
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Project description:Development of cirrhosis and hepatocellular carcinoma is main dangerous consequences of Hepatitis B virus (HBV) infection. Although a lot of data accumulated about host's immune response against infected hepatocytes, less is known about direct pathogenic effects of HBV proteins. Here we have investigated pathological outcomes of HBV envelope polypeptides expression in the liver of transgenic mice. Expression of HBV proteins induced endoplasmic reticulum (ER) stress response in hepatocytes. ER stress response included activation of PKR-like ER-localized eukaryotic initiation factor 2α (eIF2α) kinase (PERK) and eIF2α phosphorylation. In young transgenic mice on BALB/c genetic background eIF2α phosphorylation resulted in activation of GADD153/CHOP-dependent apoptosis that led to stronger liver injury and fibrosis compared to transgenic mice on C57BL/6 genetic background. Hepatic stellate cells represented the main collagen-producing cells in the liver of HBV transgenic mice. Further, key regulator of hepatocytes proliferation transcription factor c-Jun was up-regulated and this up-regulation was accompanied by c-Jun N-terminal kinases (JNK) activation in the liver of HBV transgenic mice. Thus, HBV envelope polypeptides induced host genetic background-dependent liver injury and fibrosis, and, more important, stimulated c-Jun expression and activated PERK genetic background-independent creating conditions in the liver that promote cancer cell proliferation and tumour growth.
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