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HOME > J. Microbiol > Volume 54(7); 2016 > Article
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Hepatitis C virus infection stimulates transforming growth factor-β1 expression through up-regulating miR-192
Ji Hyun Kim , Chang Ho Lee , Seong-Wook Lee
Journal of Microbiology 2016;54(7):520-526.
DOI: https://doi.org/10.1007/s12275-016-6240-3
Published online: June 28, 2016
Department of Molecular Biology, Research Institute of Advanced Omics, Dankook University, Yongin 16890, Republic of Korea
Corresponding author:  Seong-Wook Lee , Tel: -, 
Received: 25 May 2016   • Revised: 7 June 2016   • Accepted: 7 June 2016
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Abstract

The objective of this study was to determine the molecular mechanisms underlying chronic liver injury and fibrosis caused by hepatitis C virus (HCV). This study revealed that miR-192 expression was induced by HCV infection without affecting viral replication. However, viral-induced miR-192 up-regulated transforming growth factor-β1 (TGF-β1) expression in liver cells at transcriptional level. TGF-β1 stimulation by HCV-induced miR-192 was caused through ZEB1 down-regulation and TGF-β1 increased miR-192 level via positive feedback pathway. Increase in miR-192 expression by HCV infection was due to HCV core protein released and/or expressed by viral infection. TGF-β1 promoter activity was also increased by HCV core protein in liver cells. Taken together, HCV infection resulted in increased TGF-β1 transcription in hepatocytes through ZEB1 down-regulation by HCV core-mediated miR-192 stimulation. Importantly, miR-192 inhibition with anti-miR-192 rescued ZEB1 expression down-regulated by HCV infection, thus reducing the level of TGF-β1 expression increased by HCV infection in hepatocytes. These results suggest a novel mechanism of HCV-mediated liver fibrogenesis with miR-192 being a potential molecular target to ameliorate viral pathogenesis.

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    Hepatitis C virus infection stimulates transforming growth factor-β1 expression through up-regulating miR-192
    J. Microbiol. 2016;54(7):520-526.   Published online June 28, 2016
    DOI: https://doi.org/10.1007/s12275-016-6240-3
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