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Analysis of micorRNA expression during the HBV acute and chronic infections

ABSTRACT: Recent implication of microRNAs (miRNAs) in the intricate cross-talk between the host and the pathogen in viral infections reveals a new layer of mechanism for host-virus interactions. In the present study, we investigated human miRNAs which may be involved in the acute and chronic HBV infections via microarray profiling. We determined the global miRNA expression profiles elicited in the uninfected control model (HepG2), the acute infection model (HepG2 transfected with a 1.3 full-length HBV genome) and the chronic infection model (HepG2.2.15) using CapitalBio corporation’s mammalian miRNA arrays.

ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens

PROVIDER: GSE22378 | GEO | 2010/06/17

SECONDARY ACCESSION(S): PRJNA127645

REPOSITORIES: GEO

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Analysis of micorRNA expression during the HBV acute and chronic infections

Project description:Recent implication of microRNAs (miRNAs) in the intricate cross-talk between the host and the pathogen in viral infections reveals a new layer of mechanism for host-virus interactions. In the present study, we investigated human miRNAs which may be involved in the acute and chronic HBV infections via microarray profiling. We determined the global miRNA expression profiles elicited in the uninfected control model (HepG2), the acute infection model (HepG2 transfected with a 1.3 full-length HBV genome) and the chronic infection model (HepG2.2.15) using CapitalBio corporation’s mammalian miRNA arrays. Three cellular models were used in this study: the human hepatoblastoma cell line HepG2 as a blank control representing the condition without virus infection; HepG2 transfected with a 1.3 full-length HBV genome as an acute infection model; and HepG2.2.15, a well-established cell line derived from HepG2 transfected with a full-length HBV genome and constitutively expressing HBV, as a chronic infection model.

2010-06-16 | E-GEOD-22378 | biostudies-arrayexpress

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

Project description:MiRNAs are important posttranscriptional regulators in various physiological processes and their dysregulations have been found in diseases such as infection, imflammation and cancer. Here we compared the miRNA profilings between HBV-producing HepG2.2.15 and its non-HBV maternal HepG2 cell to find potential miRNAs involving in HBV expression. The result indicated that some of the deregulated miRNAs in HepG2.2.15 have been implicated in viral infection and the processes of the immune regulation. HepG2.2.15 vs. HepG2

2011-01-14 | E-GEOD-19980 | biostudies-arrayexpress

MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells.

Project description:Deficient DNA repair capacity is associated with genetic lesions accumulation and susceptibility to carcinogenesis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate various cellular pathways including DNA repair. Here we hypothesized that the existence of HBV products may interfere with cellular nucleotide excision repair (NER) through microRNA-mediated gene regulation. We found that NER was impaired in HepG2.2.15 cells, a stable HBV-expressing cell line, compared with its parental cell line HepG2. Altered miRNA expression profile, in particular the significant upregulation of miR-192, was observed in HepG2.2.15 cells. Additionally, ERCC3 and ERCC4, two key factors implicated in NER, were identified as targets of miR-192 and over-expressing miR-192 significantly inhibited cellular NER. These results indicated that persistent HBV infection might trigger NER impairment in part through upregulation of miR-192, which suppressed the levels of ERCC3 and ERCC4. It provides new insight into the effect of chronic HBV infection on NER and genetic instability in cancer. A genome-wide miRNAs microarray was performed to identify differentially expressed miRNAs between HepG2.2.15, a stable HBV-expressing cell line, and its parental cell line HepG2.

2011-08-02 | E-GEOD-27561 | biostudies-arrayexpress

The Co-regulated Genes by Ectopic Expression of MiR-371-372-373 Cluster in HepG2 Cells

Project description:MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate. miR-371-372-373-HepG2 vs. mock-HepG2

2012-01-15 | E-GEOD-19981 | biostudies-arrayexpress

The Co-regulated Genes by Ectopic Expression of MiR-371-372-373 Cluster in HepG2 Cells

2012-01-15 | GSE19981 | GEO

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

2011-01-14 | GSE19980 | GEO

Genome-wide analysis of histone methylation reveals chromatin state-based regulation of host cellular gene expression induced by hepatitis B viruses (ChIP-Seq dataset)

Project description:Hepatitis B virus (HBV) is a hepatotropic virus that can regulate many host cellular gene expressions participating in the HBV life cycle, liver inflammation and hepatocellular injury. However, the underlying mechanism of differential gene expression is not understood. We report here a genome-wide analysis of histone methylation on two histone H3 lysine residues (H3K4me3 and H3K27me3) and gene expression profiles in HepG2 and HepG2.2.15 cells. We found that specific correlation exists between gene expression and the amounts of H3K4me3 (positive correlation) and H3K27me3 (negative correlation) across the gene body. These correlations displayed three distinct modes (repressive, active and poised), reflecting different functions of these genes in the HBV life cycle, liver inflammation and hepatocellular injury. Furthermore, a permissive chromatin state of each gene was established by a combination of different histone modifications. Our findings reveal a complex regulation by histone methylation in differential gene expression and suggest that histone methylation may be responsible for the HBV life cycle, liver inflammation and hepatocellular injury induced by HBV. Examination of 2 different histone modifications (H3K4me3, H3K27me3) in 2 cell types (HepG2, HepG2.2.15).

2012-08-01 | E-GEOD-35462 | biostudies-arrayexpress

Genome-wide analysis of histone methylation reveals chromatin state-based regulation of host cellular gene expression induced by hepatitis B viruses (DGE dataset)

Project description:Hepatitis B virus (HBV) is a hepatotropic virus that can regulate many host cellular gene expressions participating in the HBV life cycle, liver inflammation and hepatocellular injury. However, the underlying mechanism of differential gene expression is not understood. We report here a genome-wide analysis of histone methylation on two histone H3 lysine residues (H3K4me3 and H3K27me3) and gene expression profiles in HepG2 and HepG2.2.15 cells. We found that specific correlation exists between gene expression and the amounts of H3K4me3 (positive correlation) and H3K27me3 (negative correlation) across the gene body. These correlations displayed three distinct modes (repressive, active and poised), reflecting different functions of these genes in the HBV life cycle, liver inflammation and hepatocellular injury. Furthermore, a permissive chromatin state of each gene was established by a combination of different histone modifications. Our findings reveal a complex regulation by histone methylation in differential gene expression and suggest that histone methylation may be responsible for the HBV life cycle, liver inflammation and hepatocellular injury induced by HBV. A large-scale analysis of gene expression of 2 different cell types (HepG2, HepG2.2.15) using a digital gene expression (DGE) tag profiling approach.

2012-08-01 | E-GEOD-35464 | biostudies-arrayexpress

MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells.

2011-08-03 | GSE27561 | GEO

Deep Characterization of the IFN-I/III-Stimulated Proteome in HBV-Transfected or Native HepG2 Cells

Project description:To expand knowledge of the effects of interferon at the proteomic level, we treated HepG2 cells with IFN-alpha and IFN-lambda for 24 hours. HepG2.2.15 cells, a model for HBV infection, were also examined versus controls. MTT assays showed that optimized IFN levels (100 ng/ml) did not induce apoptosis relative to untreated controls. Including controls, more than 6,000 proteins were identified. Five replicates each of IFN-alpha treatment, IFN-lambda treatment, and control were performed, allowing confident identification of differentially expressed proteins. While a number of publications suggest that no interferon effect is evident upon HBV infection, our own results strongly suggest otherwise. Differential alterations of the proteasome were noted when comparing HBV infection against IFN-treatment. We also note that differential effects upon IFN treatment significantly overlapped with transcriptomic datasets when upregulation was examined. However, proteins downregulated upon IFN treatment show little overlap with these transcriptomic datasets.

2020-06-26 | PXD017251 | Pride

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