國家衛生研究院 NHRI:Item 3990099045/6235
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    题名: Transforming growth factor-beta1 suppresses hepatitis B virus replication by the reduction of hepatocyte nuclear factor-4alpha expression
    其它题名: Transforming growth factor-beta1 suppresses hepatitis B virus replication by the reduction of hepatocyte nuclear factor-4α expression
    作者: Hong, MH;Chou, YC;Wu, YC;Tsai, KN;Hu, Cp;Jeng, KS;Chen, ML;Chang, CM
    贡献者: Institute of Molecular and Genomic Medicine
    摘要: Several studies have demonstrated that cytokine-mediated noncytopathic suppression of hepatitis B virus (HBV) replication may provide an alternative therapeutic strategy for the treatment of chronic hepatitis B infection. In our previous study, we showed that transforming growth factor-beta1 (TGF-β1) could effectively suppress HBV replication at physiological concentrations. Here, we provide more evidence that TGF-β1 specifically diminishes HBV core promoter activity, which subsequently results in a reduction in the level of viral pregenomic RNA (pgRNA), core protein (HBc), nucleocapsid, and consequently suppresses HBV replication. The hepatocyte nuclear factor 4alpha (HNF-4α) binding element(s) within the HBV core promoter region was characterized to be responsive for the inhibitory effect of TGF-β1 on HBV regulation. Furthermore, we found that TGF-β1 treatment significantly repressed HNF-4α expression at both mRNA and protein levels. We demonstrated that RNAi-mediated depletion of HNF-4α was sufficient to reduce HBc synthesis as TGF-β1 did. Prevention of HNF-4α degradation by treating with proteasome inhibitor MG132 also prevented the inhibitory effect of TGF-β1. Finally, we confirmed that HBV replication could be rescued by ectopic expression of HNF-4α in TGF-β1-treated cells. Our data clarify the mechanism by which TGF-β1 suppresses HBV replication, primarily through modulating the expression of HNF-4α gene.
    日期: 2012-01
    關聯: PLoS ONE. 2012 Jan;7(1):Article number e30360.
    Link to: http://dx.doi.org/10.1371/journal.pone.0030360
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1932-6203&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000301568100038
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84856035448
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