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Reham M Dawood, Mai Abd El-Meguid, Marwa K Ibrahim, Noha G Bader El Din, Ahmed Barakat, Khaled El-Wakeel, Mohamed Darwish Ahmed Abd Alla, George Y Wu, Mostafa K El Awady
BACKGROUND: Liver fibrosis results from a wound healing response to chronic injury, which leads to excessive matrix deposition. Genome wide association studies have showen transcriptional dysregulation in mild and severe liver fibrosis. Recent studies suggested that genetic markers may be able to define the exact stage of liver fibrosis. AIM: To define genes or genetic pathways that could serve as markers for staging or as therapeutic targets to halt progression of liver fibrosis...
April 20, 2018: Gene
Chee-Hing Yang, Hui-Chun Li, Tzu-Shan Ku, Pi-Ching Wu, Yung-Ju Yeh, Ju-Chien Cheng, Teng-Yi Lin, Shih-Yen Lo
Identification of host factors involved in viral replication is critical for understanding the molecular mechanism of viral replication and pathogenesis. Genes differentially expressed in HuH-7 cells with or without a hepatitis C virus (HCV) sub-genomic replicon were screened by microarray analysis. SERPINE1/PAI-1 was found to be down-regulated after HCV infection in this analysis. Down-regulation of SERPINE1/PAI-1 expression at the transcriptional level was verified by the real-time reverse transcriptase (RT)-PCR assay...
September 2017: Journal of General Virology
Dong-Mei Zou, Wan-Ling Sun
OBJECTIVE: The aim of this study was to summarize the interactions between hepatitis C virus (HCV) infection and iron overload, and to understand the mechanisms of iron overload in chronic hepatitis C (CHC) and the role iron plays in HCV life cycle. DATA SOURCES: This review was based on data in articles published in the PubMed databases up to January 28, 2017, with the keywords "hepatitis C virus", "iron overload", "iron metabolism", "hepcidin", "translation", and "replication"...
April 5, 2017: Chinese Medical Journal
Anna Kakehashi, Vasily E Stefanov, Naomi Ishii, Takahiro Okuno, Hideki Fujii, Kazuaki Kawai, Norifumi Kawada, Hideki Wanibuchi
To uncover mechanisms of nonalcoholic steatohepatitis (NASH) associated hepatocarcinogenesis, we compared the proteomes of human NASH-associated liver biopsies, resected hepatocellular carcinomas (HCCs) and HCCs of HCV⁺ patients with normal liver tissue of patients with gastrointestinal tumor metastasis, in formalin-fixed paraffin-embedded samples obtained after surgery in our hospital during the period from 2006 to 2011. In addition, proteome analysis of liver tumors in male STAM NASH-model mice was performed...
February 17, 2017: International Journal of Molecular Sciences
Che C Colpitts, Thomas F Baumert
No abstract text is available yet for this article.
January 2017: Gastroenterology
Fang Zhang, Catherine Sodroski, Helen Cha, Qisheng Li, T Jake Liang
BACKGROUND & AIMS: The signaling molecule and transcriptional regulator SMAD6, which inhibits the transforming growth factor β signaling pathway, is required for infection of hepatocytes by hepatitis C virus (HCV). We investigated the mechanisms by which SMAD6 and another inhibitory SMAD (SMAD7) promote HCV infection in human hepatoma cells and hepatocytes. METHODS: We infected Huh7 and Huh7.5.1 cells and primary human hepatocytes with Japanese fulminant hepatitis-1 (JFH1) HCV cell culture system (HCVcc)...
January 2017: Gastroenterology
Nikoletta Argentou, Georgios Germanidis, Prodromos Hytiroglou, Eirini Apostolou, Themistoklis Vassiliadis, Kalliopi Patsiaoura, Paschalis Sideras, Anastasios E Germenis, Matthaios Speletas
OBJECTIVES: Although animal studies demonstrated that Smad7 induction ameliorates TGF-β/SMAD-mediated fibrogenesis, its role in human hepatic diseases is rather obscure. Our study explored the activation status of TGF-β/activin pathway in patients with chronic liver diseases, and how it is affected by successful antiviral treatment in chronic HBV hepatitis (CHB). METHODS: Thirty-seven CHB patients (19 with active disease, 14 completely remitted on long-term antiviral treatment and 4 with relapse after treatment withdrawal), 18 patients with chronic HCV hepatitis, 12 with non-alcoholic fatty liver disease (NAFLD), and 3 controls were enrolled in the study...
May 2016: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
Gwon-Soo Jung, Jae-Han Jeon, Yeon-Kyung Choi, Se Young Jang, Soo Young Park, Mi-Kyung Kim, Eui-Cheol Shin, Won-Il Jeong, In-Kyu Lee, Yu Na Kang, Keun-Gyu Park
BACKGROUND & AIMS: An atypical orphan nuclear receptor small heterodimer partner (SHP) is known to be regulated by AMP-activated protein kinase (AMPK). Both of them inhibit TGF-β and Smad signalling and exhibit antifibrotic activity in the liver. However, little is known about the protective effects of SHP and AMPK against hepatitis c virus (HCV)-induced hepatic fibrosis. METHODS: Levels of SHP, p-AMPK and fibrotic markers in HCV-infected human liver and in Huh-7...
October 2015: Liver International: Official Journal of the International Association for the Study of the Liver
Qisheng Li, Yong-Yuan Zhang, Stephan Chiu, Zongyi Hu, Keng-Hsin Lan, Helen Cha, Catherine Sodroski, Fang Zhang, Ching-Sheng Hsu, Emmanuel Thomas, T Jake Liang
Recent functional genomics studies including genome-wide small interfering RNA (siRNA) screens demonstrated that hepatitis C virus (HCV) exploits an extensive network of host factors for productive infection and propagation. How these co-opted host functions interact with various steps of HCV replication cycle and exert pro- or antiviral effects on HCV infection remains largely undefined. Here we present an unbiased and systematic strategy to functionally interrogate HCV host dependencies uncovered from our previous infectious HCV (HCVcc) siRNA screen...
May 2014: PLoS Pathogens
Pelagia Foka, Alexios Dimitriadis, Eleni Kyratzopoulou, Dionysios A Giannimaras, Stefania Sarno, George Simos, Urania Georgopoulou, Avgi Mamalaki
Hepatitis C virus (HCV) infection is associated with hepatic iron overload and elevated serum iron that correlate to poor antiviral responses. Hepcidin (HAMP), a 25-aa cysteine-rich liver-specific peptide, controls iron homeostasis. Its expression is up-regulated in inflammation and iron excess. HCV-mediated hepcidin regulation remains controversial. Chronic HCV patients possess relatively low hepcidin levels; however, elevated HAMP mRNA has been reported in HCV core transgenic mice and HCV replicon-expressing cells...
November 2014: Cellular and Molecular Life Sciences: CMLS
Chia-Lin Chen, Hidekazu Tsukamoto, Jian-Chang Liu, Claudine Kashiwabara, Douglas Feldman, Linda Sher, Steven Dooley, Samuel W French, Lopa Mishra, Lydia Petrovic, Joseph H Jeong, Keigo Machida
Tumor-initiating stem-like cells (TICs) are resistant to chemotherapy and associated with hepatocellular carcinoma (HCC) caused by HCV and/or alcohol-related chronic liver injury. Using HCV Tg mouse models and patients with HCC, we isolated CD133(+) TICs and identified the pluripotency marker NANOG as a direct target of TLR4, which drives the tumor-initiating activity of TICs. These TLR4/NANOG-dependent TICs were defective in the TGF-β tumor suppressor pathway. Functional oncogene screening of a TIC cDNA library identified Yap1 and Igf2bp3 as NANOG-dependent genes that inactivate TGF-β signaling...
July 2013: Journal of Clinical Investigation
Amandine Verga-Gérard, Marine Porcherot, Laurène Meyniel-Schicklin, Patrice André, Vincent Lotteau, Laure Perrin-Cocon
TGF-β signaling induces epithelial to mesenchymal transition (EMT) and plays an important role in hepatocellular carcinoma (HCC) development. Clinical observations indicate that hepatitis C virus (HCV) chronic infection, which is a major cause of HCC, induces TGF-β signaling perturbations. Here, we investigate the mechanisms by which HCV nonstructural proteins interfere with TGF-β signaling, in human hepatoma cell lines expressing HCV subgenomic replicon. A transcriptomic study showed that TGF-β stimulation of these cells resulted in a protumoral gene expression profile and in up-regulation of EMT-related genes compared to control interferon-treated cells not expressing HCV proteins...
October 2013: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Takashi Yamaguchi, Koichi Matsuzaki, Ryosuke Inokuchi, Rinako Kawamura, Katsunori Yoshida, Miki Murata, Junichi Fujisawa, Nobuyoshi Fukushima, Michio Sata, Masayoshi Kage, Osamu Nakashima, Akihiro Tamori, Norifumi Kawada, Koichi Tsuneyama, Steven Dooley, Toshihito Seki, Kazuichi Okazaki
AIM: Insight into hepatic fibrogenesis and carcinogenesis (fibro-carcinogenesis) caused by hepatitis C virus (HCV) infection has come from recent analyses of transforming growth factor (TGF)-β signaling. TGF-β type I receptor and pro-inflammatory cytokine-activated kinases differentially phosphorylate Smad2 and Smad3 to create C-terminally (C), linker (L) or dually (L/C) phosphorylated (p) isoforms. This study aimed to elucidate how HCV infection affected hepatic fibro-carcinogenesis, particularly via phospho-Smad signaling...
February 20, 2013: Hepatology Research: the Official Journal of the Japan Society of Hepatology
Tirumuru Nagaraja, Li Chen, Anuradha Balasubramanian, Jerome E Groopman, Kalpana Ghoshal, Samson T Jacob, Andrew Leask, David R Brigstock, Appakkudal R Anand, Ramesh K Ganju
BACKGROUND: The pro-fibrogenic cytokine connective tissue growth factor (CTGF) plays an important role in the development and progression of fibrosis in many organ systems, including liver. However, its role in the pathogenesis of hepatitis C virus (HCV)-induced liver fibrosis remains unclear. METHODS: In the present study, we assessed CTGF expression in HCV-infected hepatocytes using replicon cells containing full-length HCV genotype 1 and the infectious HCV clone JFH1 (HCV genotype 2) by real-time PCR, Western blot analysis and confocal microscopy...
2012: PloS One
Antonios Katsounas, Martin Trippler, Shyam Kottilil, Richard A Lempicki, Guido Gerken, Joerg F Schlaak
BACKGROUND: In chronic hepatitis C virus (HCV) infection, liver tissue pathology and HCV genotype are important determinants of clinical and/or treatment-related outcome. Although consistent epidemiological and/or molecular-biological clues derived from different studies on single virus-host interactions are meanwhile published, the in vivo transcriptional responses and cellular pathways affected in >1 key aspects of the disease or treatment process are far from being understood. METHODS: Microarray analysis was performed in peripheral whole blood (PB) samples from 36 therapy-naïve HCV-infected patients with known liver histology...
2012: European Journal of Medical Research
Takayuki Murata, Takayuki Ohshima, Masashi Yamaji, Masahiro Hosaka, Yusuke Miyanari, Makoto Hijikata, Kunitada Shimotohno
Hepatitis C virus (HCV) is one of the major causative agents of liver diseases, such as liver inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. Using an efficient HCV subgenomic replicon system, we demonstrate that transforming growth factor-beta (TGF-beta) suppresses viral RNA replication and protein expression from the HCV replicon. We further show that the anti-viral effect of this cytokine is associated with cellular growth arrest in a manner dependent on Smad signaling, not mitogen-activated protein kinase (MAPK) signaling...
January 20, 2005: Virology
Fiorella Calabrese, Marialuisa Valente, Cinzia Giacometti, Elena Pettenazzo, Luisa Benvegnu, Alfredo Alberti, Angelo Gatta, Patrizia Pontisso
BACKGROUND AND AIMS: Transforming growth factor-beta (TGF-beta) system is involved in the control of cell growth and extracellular matrix formation. Previous studies in patients with chronic liver disease have shown that increased TGF-beta expression significantly correlates with the degree of hepatic fibrosis. The aim of our study was to define TGF-beta system expression in hepatic parenchymal cells and its significance in patients with differing extents of chronic liver disease of viral etiology...
November 2003: Journal of Gastroenterology and Hepatology
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