Activation of sterol regulatory element-binding protein 1c and fatty acid synthase transcription by hepatitis C virus non-structural protein 2

DOI Web Site PubMed 被引用文献2件 オープンアクセス
  • Jae-Ku Oem
    Vaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada
  • Candice Jackel-Cram
    Vaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada
  • Yi-Ping Li
    Vaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada
  • Yan Zhou
    Vaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada
  • Jin Zhong
    Institut Pasteur of Shanghai, Shanghai, PR China
  • Hitoshi Shimano
    University of Tsukuba, Tsukuba City, Ibaraki, Japan
  • Lorne A. Babiuk
    University of Alberta, Edmonton, Alberta, Canada
  • Qiang Liu
    Vaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada

書誌事項

公開日
2008-05-01
DOI
  • 10.1099/vir.0.83491-0
公開者
Microbiology Society

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説明

<jats:p>Transcriptional factor sterol regulatory element-binding protein 1c (SREBP-1c) activates the transcription of lipogenic genes, including fatty acid synthase (FAS). Hepatitis C virus (HCV) infection is often associated with lipid accumulation within the liver, known as steatosis in the clinic. The molecular mechanisms of HCV-associated steatosis are not well characterized. Here, we showed that HCV non-structural protein 2 (NS2) activated SREBP-1c transcription in human hepatic Huh-7 cells as measured by using a human SREBP-1c promoter–luciferase reporter plasmid. We further showed that sterol regulatory element (SRE) and liver X receptor element (LXRE) in the SREBP-1c promoter were involved in SREBP-1c activation by HCV NS2. Furthermore, expression of HCV NS2 resulted in the upregulation of FAS transcription. We also showed that FAS upregulation by HCV NS2 was SREBP-1-dependent since deleting the SRE sequence in a FAS promoter and expressing a dominant-negative SREBP-1 abrogated FAS promoter upregulation by HCV NS2. Taken together, our results suggest that HCV NS2 can upregulate the transcription of SREBP-1c and FAS, and thus is probably a contributing factor for HCV-associated steatosis.</jats:p>

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