Project description:We performed miRNA array analysis for S-HCV (short-term HCV), L-HCV (long-term HCV) and control (uninfected Huh751), total for 3 samples to identify miRNA candidates in HCV-related HCC.
Project description:In this study, Solexa deep sequencing technology was used for high-throughput analysis of miRNAs in a small RNA library isolated from serum sample of HCV-related fibrosis and control healthy. In total, 41 miRNAs were dysregulated (30 upregulated and 11 downregulated) in the patients with chronic HCV infection compared with the healthy controls. Furthermore, miRNA features including length distribution and end variations were characterized. Annotation of targets revealed a broad range of biological processes and signal transduction pathways regulated by HCV-induced fibrosis miRNAs. In addition, miRNAs of HCV-related fibrosis and control healthy were confirmed using miRNA microarray analysis. Real-time quantitative PCR (qPCR) analysis of miRNA in the chronic HCV infection patients and control healthy groups showed good concordance between the sequencing and qPCR data. This study provides the first large-scale identification and characterization of HCV-related fibrosis miRNAs and their potential targets, and represents a foundation for further characterization of their roles in the regulation of the diversity of HCV-related fibrosis.
Project description:A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS. A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS.
Project description:A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS. A quantitative label-free proteome analysis was performed using plasma samples from 22 hepatitis-C virus (HCV)-induced liver cirrhosis patients, 16 HCV-positive hepatocellular carcinoma patients with underlying cirrhosis and 18 healthy controls. Plasma microparticles (PMPS) were isolated using ultracentrifugation and analyzed via label-free LC-MS/MS.
Project description:A miRNA microarray was performed from HCV infected patient serum samples of bothe genotype 1b and genotype 3a, which are prevalent in India, with the aim of identifying a set of miRNAs which are uniquely differentially expressed during HCV infection. miR-320c, miR-483-5p, miR-134 and miR-198 were found to be upregulated in the patient samples as compared to the controls and are currenty being validated.
Project description:A miRNA microarray was performed from HCV infected patient serum samples of bothe genotype 1b and genotype 3a, which are prevalent in India, with the aim of identifying a set of miRNAs which are uniquely differentially expressed during HCV infection. miR-320c, miR-483-5p, miR-134 and miR-198 were found to be upregulated in the patient samples as compared to the controls and are currenty being validated. Agilent one-color experiment, Organism: Homo sapiens , Agilent Human miRNA 8x15k Arrays AMADID: 021827 [Agilent miRNA labeling reagent and Hybridization Kit Cat # 5190-0408]
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.
Project description:Introduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip™ System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis. Keywords: HCV-advance disease state