Abstract
We have examined the underlying mechanism of hepatitis C virus (HCV)-mediated IFITM1 regulation. IFITM1 is a potential target of miR-130a. Our results demonstrated that miR-130a expression was significantly higher in HCV-infected hepatocytes and liver biopsy specimens than in controls. Introduction of anti-miR-130a in hepatocytes increased IFITM1 expression. Hepatocytes stably expressing IFITM1 reduced HCV replication. Together, these results suggested that HCV infection of hepatocytes upregulates miR-130a and that use of anti-miR-130a may have potential for restriction of HCV replication.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Antigens, Differentiation / genetics*
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Base Sequence
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Cell Line
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Gene Knockdown Techniques
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Hepacivirus / genetics
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Hepacivirus / immunology
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Hepacivirus / pathogenicity*
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Hepacivirus / physiology
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Hepatitis C / genetics*
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Hepatitis C / immunology*
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Hepatitis C / virology
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Hepatocytes / immunology
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Hepatocytes / virology
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Host-Parasite Interactions / genetics
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Host-Parasite Interactions / immunology
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Humans
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MicroRNAs / antagonists & inhibitors
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MicroRNAs / genetics*
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RNA, Viral / biosynthesis
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RNA, Viral / genetics
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Up-Regulation
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Virus Replication
Substances
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Antigens, Differentiation
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MIRN130 microRNA, human
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MicroRNAs
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RNA, Viral
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leu-13 antigen