Expression data from transgenic mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE84429 | GEO | 2016/07/15
SECONDARY ACCESSION(S): PRJNA329136
REPOSITORIES: GEO
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Project description:This study aimed to evaluate the change of liver status in the presence of hepatitis B viral proteins We evaluated the messenger RNA expression profiles of liver tissues of transgenic mices carrying wild type or mutant viral surface proteins We checked the differential RNA expressions in different transgenic mice, each with three biological replicates
2016-07-15 | E-GEOD-84429 | biostudies-arrayexpress
Project description:This study aimed to evaluate the change of liver status in the presence of hepatitis B viral proteins We evaluated the microRNA expression profiles of liver tissues of transgenic mices carrying wild type or mutant viral surface proteins
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Project description:We have performed a genome wide transcriptional survey of liver biopsies obtained from patients in Hunan China, who have chronic schistosomiasis with and without past viral hepatitis history, compared to patients with no liver disease history or indicators. These results present a comprehensive transcriptional profile of chronic schistosomiasis japonica patients and demonstrate similarities and differences with other hepatic diseases. These unique features of gene expression, in conjunction with previous reports of the cellular composition of granuloma formation and recovery, present an improved understanding of the molecular immunopathology and general physiological status underlying hepatic schistosomiasis. The gene expression profile of the human liver was examined for chronic patients with Schistosoma japonicum infections. Microarray analysis was performed on cRNA synthesised from total RNA derived from the liver biopsy tissue from huan China. Three groups were examined based on infections status [C] were without history or indicators of schistosomiasis or viral heapatitis controls ; [S] with a history or active for schistosomiasis but no indicators of viral heapatitis; and [S]
2014-09-13 | E-GEOD-61376 | biostudies-arrayexpress
Project description:Small, non-coding RNAs control gene expression post-transcriptionally and play important roles in virus-host interactions. Within the liver, the microRNA (miRNA) miR-122 is essential for replication of hepatitis C virus (HCV), while repression of miR-148a by hepatitis B virus (HBV) may enhance tumorigenesis. Despite their importance to the outcome of these infections, few previous studies have described unbiased profiling of small RNAs in the liver during chronic viral hepatitis. Here, we sequenced small (14-40 nts) RNAs in liver from subjects with chronic hepatitis B and C. We found that small RNAs derived from tRNAs, specifically 5’ tRNA-halves (“5’ tRHs”, ~31-34 nts), are abundant in liver and significantly increased during chronic viral infection in humans and also chimpanzees. In most infected livers, 5’ tRH abundance exceeded that of miRNAs. In contrast, in hepatocellular carcinoma (HCC) tissue from these subjects, tRH abundance was reduced concomitant with decreased expression of the tRNA-cleaving ribonuclease, angiogenin. Although tRHs have been identified in mice, our results show they are abundantly expressed in human tissue, increased in chronic viral infection, and decreased in liver cancer. Our findings highlight the potential biological and clinical relevance of these small non-coding RNAs. Small RNA-seq of liver samples from control subjects (n=4), subjects with chronic hepatitis B (n=4) and hepatitis B associated hepatocellular carcinoma (n=4, 3 out of 4 matched with non-tumor tissue) and subjects with chronic hepatitis C (n=4) and tissue from hepatocellular carcinoma of the same patients. Also, small RNA-seq of AGO2 and IgG pulldown in FT3-7 cells. Sequenced AGO2 pulldown (n=3), IgG pulldown (n=2) and total small RNA from FT3-7 cells (n=3). This dataset is part of the TransQST collection.
2014-12-18 | E-GEOD-57381 | biostudies-arrayexpress
Project description:We have performed a genome wide transcriptional survey of liver biopsies obtained from patients in Hunan China, who have chronic schistosomiasis with and without past viral hepatitis history, compared to patients with no liver disease history or indicators. These results present a comprehensive transcriptional profile of chronic schistosomiasis japonica patients and demonstrate similarities and differences with other hepatic diseases. These unique features of gene expression, in conjunction with previous reports of the cellular composition of granuloma formation and recovery, present an improved understanding of the molecular immunopathology and general physiological status underlying hepatic schistosomiasis.
2014-09-13 | GSE61376 | GEO
Project description:Hepatitis B virus (HBV) is an enveloped, coated, non-cytopathic and hepatotropic partially double-stranded DNA virus in the family Hepadnaviridae genus Orthohepadnavirus. Despite significant progress in the availability of safe vaccines and antiviral therapies against HBV, it still affects approximately 257 million people worldwide and is responsible for about 887,000 deaths per year around the world [4]. HBV infection, which are associated with acute and chronic liver failure responses to viruses attacked the liver, can result in inactive carrier state, chronic hepatitis, or fulminant hepatitis and put them at high risk to develop advanced liver fibrosis and cirrhosis, and even hepatocellular cancer. Many viral factors, which could affect the disparity of clinical outcomes or disease prognosis during chronic HBV infection, have been reported in previous studies; among them, the viral genotype, as well as HBV mutations ascribing the virus to a certain phenotype, was reported to be the most important factor influencing viral pathogenesis, including the change of host immune recognition, the enhanced virulence with increased HBV replication and the facilitation of cell attachment or penetration.
2022-02-17 | PXD025968 | Pride
Project description:Hepatitis C virus (HCV) infection has been successfully managed by anti-viral therapies, however, high prevalence to severe chronic liver disease state including non-alcoholic fatty liver disease (NAFLD) is a problem encountered even after the cure of hepatitis C. Moreover, there is currently no reliable in vitro model capable of investigating host-viral interactions and monitoring the progression of viral hepatitis to chronic liver diseases. Recent organoid technology has been reported for successful infection of HCV, but there is still lack of non-parenchymal cells, which play a crucial role in disease progression. Here, we provided a novel multicellular liver organoid model using co-culture system of macrophages and liver organoids differentiated from the same cell source, human embryonic stem cells. Surprisingly, HCV infection led potent lipid accumulation in liver organoids through regulation of host lipid metabolism, which was further promoted by macrophage co-culture. Lipid enriched condition provided by longterm-treatment with fatty acid accelerated potent HCV amplification and further promotion of inflammation and fibrosis progression. Therefore, our model may be a valuable novel platform recapitulating diverse phenotypes with host-virus intercommunication and inter-cellular interactions and further progressive features of hepatitis C-associated chronic NAFLD progression of patients with HCV.
2024-05-05 | GSE229608 | GEO
Project description:Hepatitis C virus (HCV) infection has been successfully managed by anti-viral therapies, however, high prevalence to severe chronic liver disease state including non-alcoholic fatty liver disease (NAFLD) is a problem encountered even after the cure of hepatitis C. Moreover, there is currently no reliable in vitro model capable of investigating host-viral interactions and monitoring the progression of viral hepatitis to chronic liver diseases. Recent organoid technology has been reported for successful infection of HCV, but there is still lack of non-parenchymal cells, which play a crucial role in disease progression. Here, we provided a novel multicellular liver organoid model using co-culture system of macrophages and liver organoids differentiated from the same cell source, human embryonic stem cells. Surprisingly, HCV infection led potent lipid accumulation in liver organoids through regulation of host lipid metabolism, which was further promoted by macrophage co-culture. Lipid enriched condition provided by longterm-treatment with fatty acid accelerated potent HCV amplification and further promotion of inflammation and fibrosis progression. Therefore, our model may be a valuable novel platform recapitulating diverse phenotypes with host-virus intercommunication and inter-cellular interactions and further progressive features of hepatitis C-associated chronic NAFLD progression of patients with HCV.
2024-05-05 | GSE229596 | GEO
Project description:We perform genome wide methylation analysis using 33 clinical samples, which were obtained from patients who underwent surgical resection at the Aichi Cancer Center Hospital in accordance with institutional policies. The purpose of this experiment is revealing the methylation status affected by hepatitis viral infection.
2014-01-03 | E-MTAB-1472 | biostudies-arrayexpress
Project description:BACKGROUND: Hepatocellular carcinoma (HCC) is a common complication of chronic viral hepatitis. In support of this notion, we have reported that hepatitis B surface antigen (HBsAg)-specific CD8+ T lymphocytes critically contribute to inducing chronic liver cell injury that exerts high carcinogenic potential in a hepatitis B virus (HBV) Tg mouse model. The dynamics of the molecular signatures responsible for hepatocellular carcinogenesis are not fully understood. The current study was designed to determine the serial changes in gene expression profiles in a model of chronic immune-mediated hepatitis. METHODS: Three-month-old HBV Tg mice were immunologically reconstituted with bone marrow cells and splenocytes from syngeneic nonTg donors. Liver tissues were obtained every three months until 18 months at which time all mice developed multiple liver tumors. Nitrative DNA lesions and hepatocyte turnover were assessed immunohistochemically. Gene expression profiles were generated by extracting total RNA from the tissues and analyzing by microarray. RESULTS: The nitrative DNA lesions and the regenerative proliferation of hepatocytes were increased during the progression of chronic liver disease. In a gene expression profile analysis of liver samples, the chemokine- and T cell receptor (TCR)-mediated pathways were enhanced during chronic hepatitis, and the EGF- and VEGF-mediated pathways were induced in HCC. Among these molecules, the protein levels of STAT3 were greatly enhanced in all hepatocyte nuclei and further elevated in the cytoplasm in HCC tissue samples at 18 months, and the levels of phosphorylated TP53 (p-p53-Ser 6 and -Ser 15) were increased in liver tissues. CONCLUSIONS: HBV-specific immune responses caused unique molecular signatures in the liver tissues of chronic hepatitis and triggered subsequent carcinogenic gene expression profiles in a mouse model. The results suggest a plausible molecular basis responsible for HBV-induced immune pathogenesis of HCC.
2017-08-29 | GSE103205 | GEO