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Adiponectin, a downstream target gene of peroxisome proliferator-activated receptor γ, controls hepatitis B virus replication

Authors
Yoon, S; Jung, J; Kim, T; Park, S; Chwae, YJ; Shin, HJ; Kim, K
Citation
Virology, 409(2):290-298, 2011
Journal Title
Virology
ISSN
0042-68221096-0341
Abstract
In this study, HepG2-hepatitis B virus (HBV)-stable cells that did not overexpress HBx and HBx-deficient mutant-transfected cells were analyzed for their expression of HBV-induced, upregulated adipogenic and lipogenic genes. The mRNAs of CCAAT enhancer binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), adiponectin, liver X receptor α (LXRα), sterol regulatory element binding protein 1c (SREBP1c), and fatty acid synthase (FAS) were expressed at higher levels in HepG2-HBV and lamivudine-treated stable cells and HBx-deficient mutant-transfected cells than in the HepG2 cells. Lamivudine treatment reduced the mRNA levels of PPARγ and C/EBPα. Conversely, HBV replication was upregulated by adiponectin and PPARγ agonist rosiglitazone treatments and was downregulated by adiponectin siRNAs. Collectively, our results demonstrate that HBV replication and/or protein expression, even in the absence of HBx, upregulated adipogenic or lipogenic genes, and that the control of adiponectin might prove useful as a therapeutic modality for the treatment of chronic hepatitis B.
MeSH terms
Adiponectin/antagonists & inhibitors/genetics/*metabolismAntiviral Agents/pharmacologyCell LineGene Expression ProfilingGene SilencingHepatitis B virus/*physiologyHepatocytes/virology*Host-Pathogen InteractionsHumansLamivudine/pharmacologyPPAR gamma/antagonists & inhibitors/genetics/*metabolism*Virus Replication
DOI
10.1016/j.virol.2010.10.024
PMID
21059469
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
윤, 사라박, 선최, 용준신, 호준김, 경민
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