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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome study of hepatocytes isolated from transgenic mice expressing HCV core.

ABSTRACT: Hepatitis C Virus (HCV) core protein plays a major role in HCV mediated liver pathologies. We have previously reported that HCV core variants isolated from tumoral (T) and non-tumoral (NT) livers were capable to alleviate Smad transcriptional activity and to shift TGF-β responses from tumor suppressor effects to tumor promotion. To comprehensively appreciate the consequences of core-mediated deregulation of Smad signaling on TGF-b target gene expression, Affimetrix microarrays were performed. Microarray analyses demonstrate that HCV core expression in hepatocytes modulates TGF-b target gene expression. Furthermore, most of the genes modulated in core expressing hepatocytes after TGF-b treatment were already regulated in these non treated cells suggesting that HCV core is capable to activate latent TGF-b. Transcriptome analysis was performed on primary hepatocytes from transgenic mice expressing either Core T or core NT or their control littermates treated or not with TGF-b.

ORGANISM(S): Mus musculus

SUBMITTER: christophe desterke

PROVIDER: E-GEOD-36220 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptome study of hepatocytes isolated from transgenic mice expressing HCV core.

Project description:Hepatitis C Virus (HCV) core protein plays a major role in HCV mediated liver pathologies. We have previously reported that HCV core variants isolated from tumoral (T) and non-tumoral (NT) livers were capable to alleviate Smad transcriptional activity and to shift TGF-β responses from tumor suppressor effects to tumor promotion. To comprehensively appreciate the consequences of core-mediated deregulation of Smad signaling on TGF-b target gene expression, Affimetrix microarrays were performed. Microarray analyses demonstrate that HCV core expression in hepatocytes modulates TGF-b target gene expression. Furthermore, most of the genes modulated in core expressing hepatocytes after TGF-b treatment were already regulated in these non treated cells suggesting that HCV core is capable to activate latent TGF-b.

2012-03-03 | GSE36220 | GEO

Transcriptomic analysis of HCV+ vs HCV- hepatocytes and tumoral cells

Project description:HCV+ cells were detected by smiFISH on liver section of a patient with hepatocellular carcinoma. Clusters of HCV+ and HCV- cells were captured by laser microdissection and transriptomes analysed by RNA sequening. Highly sensitive single molecule fluorescent in situ hybridization applied to frozen tissue sections of a hepatitis C patient allowed the delineation of clusters of infected hepatocytes. Laser micro-dissection followed by RNAseq analysis of HCV-positive and -negative regions from the tumoral and non-tumoral tissues from the same patient revealed HCV-related deregulation of expression of genes in the tumor and in the non-tumoral tissue.

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Transcriptomic analysis of HCV+ vs HCV- hepatocytes and tumoral cells

Project description:Transcriptomic analysis of HCV+ vs HCV- hepatocytes and tumoral cells

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Expression data from mouse hepatocellular carcinomas developed in Axin1 hepatocyte deleted mice

Project description:Mouse liver tumors (T) and non tumoral adjacent livers (NT) sorted from mice knock out for Axin1 gene specifically in the hepatocytes . 3 mice of the brother hood non deleted for Axin1 were used as controls (WT) We used microarrays to determine the differential expression between tumoral and non tumoral tissue.

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Expression data in human hepatocytes with HCV infection

Project description:Human hepatocyte chimeric mice were prepared and treated with hepatitis C virus (HCV) and/or interferon-alpha (IFN-Î±). To analyze the changes in gene expression, cDNA microarray analysis was performed with the collected human hepatocytes from the chimeric mouse livers. We consider that these results provide molecular insights into possible mechanisms used by HCV to evade innate immune responses, as well as novel therapeutic targets and a potential new indication for interferon therapy. A total of 15 human hepatocyte chimeric mice were prepared and divided into four experimental groups. Mice in group A were neither infected with HCV nor treated with IFN. Mice in group B were administered IFN-Î± 6 h before sacrifice but were not infected with HCV. The mice in groups C and D were both inoculated via the mouse tail vein with human serum containing HCV genotype 1b particles. At 8 weeks after inoculation, the mice in group D were administered IFN-Î± 6 h before sacrifice, but the mice in group C were not treated with IFN-Î±. The human hepatocytes in the mouse livers were collected after sacrifice and subjected to microarray analysis. After purification and reverse transcription of total RNA, cDNA was hybridized on Affymetrix GeneChip Human Gene U133 Plus 2.0 Arrays.

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Transcription profiling by array of mouse hepatocytes following treatment with growth factor beta 1 in a time series

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Interferon Lambda Alleles Predict Innate Antiviral Immune Responses and Hepatitis C Virus Permissiveness.

Project description:Hepatitis C virus (HCV) infection can result in viral chronicity or clearance. Although host genetics and particularly genetic variation in the interferon lambda (IFNL) locus are associated with spontaneous HCV clearance and treatment success, the mechanisms guiding these clinical outcomes remain unknown. Using a laser capture microdissection-driven unbiased systems virology approach, we isolated and transcriptionally profiled HCV-infected and adjacent primary human hepatocytes (PHH) approaching single cell resolution. An innate antiviral immune signature dominated the transcriptional response, but differed in magnitude and diversity between HCV-infected and adjacent cells. Molecular signatures associated with more effective antiviral control were determined by comparing donors with high and low infection frequencies. Cells from donors with clinically unfavorable IFNL genotypes were infected at a greater frequency and exhibited dampened antiviral and cell death responses. These data suggest that early virus-host interactions, particularly host genetics and induction of innate immunity, critically determine the outcome of HCV infection. Cell populations of primary human hepatocytes were collected via laser capture microdissection, their transcriptomes were amplified and analyzed via whole Illumina genome microarray. Three populations were collected: virus infected cells, cells adjacent to infected cells (“adjacent”) and mock infected cells. Cells from multiple donors were employed to address host genetic variability on our observed phenotypes. Nine different donors were assessed on 1-day post infection and three donors were assessed 3 days post infection and and four donors were assessed on 7 days post infection. For each cell population (virus infected, adjacent or mock), four biological replicate arrays were performed. In total, we analyzed 186 microarrays

2014-02-12 | E-GEOD-54648 | biostudies-arrayexpress

Primary Human Hepatocytes with HCVcc infection timecourse

Project description:Goal was to investigate the transcriptional effect of Hepatitis C Virus (HCV) infection upon hepatic gene expression in a primary tissue system. Cultured Primary human hepatocytes were infected with HCV (genotype 2a-JFH1) and maintained through a timecourse in parallel with matched controls of uninfected cells culture.These samples are a subset of a larger experiment to be published at a later date, which also included treatments with Type I and Type II interferons.

2015-01-31 | E-MTAB-2476 | biostudies-arrayexpress

Primary human hepatocytes treated with IFNalpha and IL28B

Project description:Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood. Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression. In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways. Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs. Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with IFN, IL28b and T-PolyC after 6 or 24 hours respectively

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Primary human hepatocytes treated with IL28B and the HCV JFH1 Genotype 2A clone.

Project description:Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood. Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression. In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways. Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs. Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with JFHA, and IL28b respectively with three biological replication.

2013-08-16 | E-GEOD-31455 | biostudies-arrayexpress

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