Discussion on differential gene expression between chronic hepatitis B and C hepatic lesion

2001 ◽  
Vol 121 (5) ◽  
pp. 1263-1264 ◽  
Author(s):  
G.W. McCaughan ◽  
N.A. Shackel ◽  
M.D. Gorrell
Keyword(s):  
Gene Expression ◽  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Differential Gene Expression ◽  
Hepatic Lesion ◽  
Differential Gene

Differential gene expression between chronic hepatitis B and C hepatic lesion

2001 ◽  
Vol 120 (4) ◽  
pp. 955-966 ◽  
Author(s):  
Masao Honda ◽  
Shuichi Kaneko ◽  
Hiroshi Kawai ◽  
Yukihiro Shirota ◽  
Kenichi Kobayashi
Keyword(s):  
Gene Expression ◽  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Differential Gene Expression ◽  
Hepatic Lesion ◽  
Differential Gene

scholarly journals Author Correction: Hypoxic gene expression in chronic hepatitis B virus infected patients is not observed in state-of-the-art in vitro and mouse infection models

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Peter Jianrui Liu ◽  
James M. Harris ◽  
Emanuele Marchi ◽  
Valentina D’Arienzo ◽  
Thomas Michler ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
State Of The Art ◽  
Infection Models ◽  
Chronic Hepatitis B Virus ◽  
B Virus

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

scholarly journals Transcriptomic Analysis of Chronic Hepatitis B and C and Liver Cancer Reveals MicroRNA-Mediated Control of Cholesterol Synthesis Programs

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Sara R. Selitsky ◽  
Timothy A. Dinh ◽  
Cynthia L. Toth ◽  
C. Lisa Kurtz ◽  
Masao Honda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Hepatitis B ◽  
Viral Hepatitis ◽  
Chronic Hepatitis B ◽  
Cholesterol Synthesis ◽  
Chronic Viral Hepatitis ◽  
Cholesterol Homeostasis ◽  
Disease States

ABSTRACT Chronic hepatitis B (CHB), chronic hepatitis C (CHC), and associated hepatocellular carcinoma (HCC) are characterized by cholesterol imbalance and dyslipidemia; however, the key regulatory drivers of these phenotypes are incompletely understood. Using gene expression microarrays and high-throughput sequencing of small RNAs, we performed integrative analysis of microRNA (miRNA) and gene expression in nonmalignant and matched cancer tissue samples from human subjects with CHB or CHC and HCC. We also carried out follow-up functional studies of specific miRNAs in a cell-based system. These studies led to four major findings. First, pathways affecting cholesterol homeostasis were among the most significantly overrepresented among genes dysregulated in chronic viral hepatitis and especially in tumor tissue. Second, for each disease state, specific miRNA signatures that included miRNAs not previously associated with chronic viral hepatitis, such as miR-1307 in CHC, were identified. Notably, a few miRNAs, including miR-27 and miR-224, were components of the miRNA signatures of all four disease states: CHB, CHC, CHB-associated HCC, and CHC-associated HCC. Third, using a statistical simulation method (miRHub) applied to the gene expression data, we identified candidate master miRNA regulators of pathways controlling cholesterol homeostasis in chronic viral hepatitis and HCC, including miR-21, miR-27, and miR-33. Last, we validated in human hepatoma cells that both miR-21 and miR-27 significantly repress cholesterol synthesis and that miR-27 does so in part through regulation of the gene that codes for the rate-limiting enzyme 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase (HMGCR). IMPORTANCE Hepatitis B virus (HBV) and hepatitis C virus (HCV) are phylogenetically unrelated hepatotropic viruses that persistently infect hundreds of millions of people world-wide, often leading to chronic liver disease and hepatocellular carcinoma (HCC). Chronic hepatitis B (CHB), chronic hepatitis C (CHC), and associated HCC often lead to cholesterol imbalance and dyslipidemia. However, the regulatory mechanisms underlying the dysregulation of lipid pathways in these disease states are incompletely understood. MicroRNAs (miRNAs) have emerged as critical modulators of lipid homeostasis. Here we use a blend of genomic, molecular, and biochemical strategies to identify key miRNAs that drive the lipid phenotypes of chronic viral hepatitis and HCC. These findings provide a panoramic view of the miRNA landscape in chronic viral hepatitis, which could contribute to the development of novel and more-effective miRNA-based therapeutic strategies.

scholarly journals Molecular Mechanisms of Same TCM Syndrome for Different Diseases and Different TCM Syndrome for Same Disease in Chronic Hepatitis B and Liver Cirrhosis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Zhizhong Guo ◽  
Shuhao Yu ◽  
Yan Guan ◽  
Ying-Ya Li ◽  
Yi-Yu Lu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Cirrhosis ◽  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Molecular Mechanisms ◽  
Molecular Feature ◽  
The Difference ◽  
Tcm Syndrome ◽  
Was Gene

Traditional Chinese medicine (TCM) treatment is based on the traditional diagnose method to distinguish the TCM syndrome, not the disease. So there is a phenomenon in the relationship between TCM syndrome and disease, called Same TCM Syndrome for Different Diseases and Different TCM Syndrome for Same Disease. In this study, we demonstrated the molecular mechanisms of this phenomenon using the microarray samples of liver-gallbladder dampness-heat syndrome (LGDHS) and liver depression and spleen deficiency syndrome (LDSDS) in the chronic hepatitis B (CHB) and liver cirrhosis (LC). The results showed that the difference between CHB and LC was gene expression level and the difference between LGDHS and LDSDS was gene coexpression in the G-protein-coupled receptor protein-signaling pathway. Therein genes GPER, PTHR1, GPR173, and SSTR1 were coexpressed in LDSDS, but not in LGDHS. Either CHB or LC was divided into the alternative LGDHS and LDSDS by the gene correlation, which reveals the molecular feature of Different TCM Syndrome for Same Disease. The alternatives LGDHS and LDSDS were divided into either CHB or LC by the gene expression level, which reveals the molecular feature of Same TCM Syndrome for Different Diseases.

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