scholarly journals Hepatitis C virus-induced CCL5 secretion from macrophages activates hepatic stellate cells

Hepatology ◽  
2017 ◽  
Vol 66 (3) ◽  
pp. 746-757 ◽  
Author(s):  
Reina Sasaki ◽  
Pradip B. Devhare ◽  
Robert Steele ◽  
Ranjit Ray ◽  
Ratna B. Ray
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatic Stellate Cells ◽  
Stellate Cells

scholarly journals Hepatitis C virus core protein induces fibrogenic actions of hepatic stellate cells via toll-like receptor 2

2011 ◽  
Vol 91 (9) ◽  
pp. 1375-1382 ◽  
Author(s):  
Martin Coenen ◽  
Hans Dieter Nischalke ◽  
Benjamin Krämer ◽  
Bettina Langhans ◽  
Andreas Glässner ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatic Stellate Cells ◽  
Core Protein ◽  
Stellate Cells ◽  
Toll Like Receptor ◽  
Virus Core ◽  
Toll Like Receptor 2

Hepatic Stellate Cells and Fibrogenesis in Hepatitis C Virus Infection: An Ultrastructural Insight

2010 ◽  
Vol 34 (2) ◽  
pp. 62-67 ◽  
Author(s):  
Soheir S. Mansy ◽  
Nagwa A. ElKhafif ◽  
Ahmed S. AbelFatah ◽  
Hoda A. Yehia ◽  
Ibrahim Mostafa
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Hepatitis C Virus Infection

386 PARACRINE ACTIVATION OF HUMAN HEPATIC STELLATE CELLS BY HEPATITIS C VIRUS VIA ANGIOPOIETIN RECEPTOR, TIE-2

2012 ◽  
Vol 56 ◽  
pp. S155
Author(s):  
S. Martin-Vilchez ◽  
Y. Rodriguez-Muñoz ◽  
R. Lopez-Rodriguez ◽  
A. Bartolome-Hernandez ◽  
R. Aldabe ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Paracrine Activation

scholarly journals Exosome-Mediated Intercellular Communication between Hepatitis C Virus-Infected Hepatocytes and Hepatic Stellate Cells

2017 ◽  
Vol 91 (6) ◽  
Author(s):  
Pradip B. Devhare ◽  
Reina Sasaki ◽  
Shubham Shrivastava ◽  
Adrian M. Di Bisceglie ◽  
Ranjit Ray ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Intercellular Communication ◽  
Hepatic Stellate Cells ◽  
Molecular Mechanisms ◽  
Stellate Cells ◽  
Hcv Infection ◽  
Marker Genes

ABSTRACT Fibrogenic pathways in the liver are principally regulated by activation of hepatic stellate cells (HSC). Fibrosis is associated with chronic hepatitis C virus (HCV) infection, although the mechanism is poorly understood. HSC comprise the major population of nonparenchymal cells in the liver. Since HCV does not replicate in HSC, we hypothesized that exosomes secreted from HCV-infected hepatocytes activate HSC. Primary or immortalized human hepatic stellate (LX2) cells were exposed to exosomes derived from HCV-infected hepatocytes (HCV-exo), and the expression of fibrosis-related genes was examined. Our results demonstrated that HCV-exo internalized to HSC and increased the expression of profibrotic markers. Further analysis suggested that HCV-exo carry miR-19a and target SOCS3 in HSC, which in turn activates the STAT3-mediated transforming growth factor β (TGF-β) signaling pathway and enhances fibrosis marker genes. The higher expression of miR-19a in exosomes was also observed from HCV-infected hepatocytes and in sera of chronic HCV patients with fibrosis compared to healthy volunteers and non-HCV-related liver disease patients with fibrosis. Together, our results demonstrated that miR-19a carried through the exosomes from HCV-infected hepatocytes activates HSC by modulating the SOCS-STAT3 axis. Our results implicated a novel mechanism of exosome-mediated intercellular communication in the activation of HSC for liver fibrosis in HCV infection. IMPORTANCE HCV-associated liver fibrosis is a critical step for end-stage liver disease progression. However, the molecular mechanisms for hepatic stellate-cell activation by HCV-infected hepatocytes are underexplored. Here, we provide a role for miR-19a carried through the exosomes in intercellular communication between HCV-infected hepatocytes and HSC in fibrogenic activation. Furthermore, we demonstrate the role of exosomal miR-19a in activation of the STAT3–TGF-β pathway in HSC. This study contributes to the understanding of intercellular communication in the pathogenesis of liver disease during HCV infection.

scholarly journals Molecular Crosstalk between the Hepatitis C Virus and the Extracellular Matrix in Liver Fibrogenesis and Early Carcinogenesis

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2270
Author(s):  
Emma Reungoat ◽  
Boyan Grigorov ◽  
Fabien Zoulim ◽  
Eve-Isabelle Pécheur
Keyword(s):  
Extracellular Matrix ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Cancer Initiation ◽  
Liver Fibrogenesis ◽  
Early Carcinogenesis ◽  
Molecular Crosstalk

Chronic infection by the hepatitis C virus (HCV) is a major cause of liver diseases, predisposing to fibrosis and hepatocellular carcinoma. Liver fibrosis is characterized by an overly abundant accumulation of components of the hepatic extracellular matrix, such as collagen and elastin, with consequences on the properties of this microenvironment and cancer initiation and growth. This review will provide an update on mechanistic concepts of HCV-related liver fibrosis/cirrhosis and early stages of carcinogenesis, with a dissection of the molecular details of the crosstalk during disease progression between hepatocytes, the extracellular matrix, and hepatic stellate cells.

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