Exosome-Mediated Intercellular Communication Is Implicated in Activation of Hepatic Stellate Cells for Liver Fibrosis in Hepatitis C Virus Infection

Hepatitis C virus (HCV)-associated liver fibrosis is a critical step for end-stage liver disease progression in chronic HCV infection. Fibrogenic pathways in the liver are principally regulated by activation of hepatic stellate cells (HSC). The mechanism underlying the liver fibrosis associated with chronic HCV infection has heretofore been poorly understood. Now, scientists at St. Louis University in Missouri have conducted experiments indicating that microRNA-19a (miR-19a) is carried by exosomes from HCV-infected hepatocytes to HSC, where the miR-19a activates the HSC to produce liver fibrosis. In the HSC, miR-19a targets SOCS3, which in turn activates the STAT3-mediated transforming growth factor-beta (TGF-beta) signaling pathway and enhances fibrosis marker genes. The authors state that “Our results implicated a novel mechanism of exosome-mediated intercellular communication in the activation of HSC for liver fibrosis in HCV infection.” These results were published in the March 2017 issue of the Journal of Virology. The article is titled “Exosome-Mediated Intercellular Communication between Hepatitis C Virus-Infected Hepatocytes and Hepatic Stellate Cells.” [Journal of Virology abstract]
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