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.
Project description:Primary human hepatocytes (PHHs) are a liver-specific cell subtype, and we have shown that these cells respond in a unique manner to the introduction of hepatitis C viral RNA (HCV vRNA) derived from different genotypes of the virus. We used microarray to analyze the transcriptional differences between the PHHs exposed to the different genotypes of HCV to further shed light on their differential effects on HCV innate immune responses in vitro HCV vRNA from either genotype 3a HCV or genotype 1a HCV was introduced into the PHH cells for 8 hours. Total RNA was then harvested to determine transcriptional differences.
Project description:Human hepatocyte chimeric mice were prepared and treated with hepatitis C virus (HCV) and/or interferon-alpha (IFN-α). 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-α 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-α 6 h before sacrifice, but the mice in group C were not treated with IFN-α. 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.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
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. 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.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.