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Title 

Hepatitis B virus X protein induces hepatic steatosis via transcriptional activation of SREBP1 and PPARγ

Authors 

K H KimHye Jun ShinK KimH M ChoiS H RheeH MoonH H KimU S YangDae Yeul YuJ Cheong

Publisher 

Elsevier

Issue Date 

2007

Citation 

Gastroenterology, vol. 132, no. 5, pp. 1955-1967

Keywords 

hepatitis B virus X proteinperoxisome proliferator activated receptor alphasterol regulatory element binding protein 1animal experimentgene expressiongene overexpressionhepatitislipid metabolismliver fibrosisprotein blood level

Abstract 

Background & Aims: Hepatic steatosis occurs frequently in patients with chronic hepatitis B virus (HBV) or chronic hepatitis C virus (HCV) infection. Recently, several studies suggested that steatosis plays an important role as a cofactor in other liver diseases such as hepatic fibrosis, hepatitis, and liver cancer. In contrast to HCV, however, the molecular mechanism by which HBV mediates hepatic steatosis has not been clearly studied. Here, we show the molecular mechanism by which hepatitis B virus X protein (HBx) induces hepatic steatosis. Methods: Lipid accumulation and the expression of various lipid metabolic genes were investigated in HBx-transfected Chang liver cells, HepG2-HBx stable cells, and HBx-transgenic mice. Results: Overexpression of HBx induced hepatic lipid accumulation in HepG2-HBx stable cells and HBx-transgenic mice. It also up-regulated the messenger RNA and protein levels of sterol regulatory element binding protein 1, but not peroxisome proliferator-activated receptor alpha (PPARα). Moreover, we also determined that the expression of HBx increases PPARγ gene expression as well as its transcriptional activity in hepatic cells, mediated by CCAAT enhancer binding protein α activation. Finally, we showed that HBx expression is able to up-regulate the gene expressions of various lipogenic and adipogenic enzymes in hepatic cells. Conclusions: We showed that the increased HBx expression causes lipid accumulation in hepatic cells mediated by sterol regulatory element binding protein 1 and PPARγ, which could be a putative molecular mechanism mediating the pathophysiology of HBV infection.

ISSN 

0016-5085

Link 

http://dx.doi.org/10.1053/j.gastro.2007.03.039

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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