Kim Kyeongjin, Kim Kook Hwan, Ha Eunsin, Park Jin Young, Sakamoto Naoya, Cheong Jaehun
Department of Molecular Biology, College of Natural Sciences, Pusan National University, Busan 609-735, Republic of Korea.
FEBS Lett. 2009 Sep 3;583(17):2720-6. doi: 10.1016/j.febslet.2009.07.034. Epub 2009 Jul 23.
Steatosis is an established risk factor for disease progression in cases of chronic hepatitis C. Recently it was demonstrated that Hepatitis C virus (HCV) core and non-structural (NS) 2 proteins (NS2) induce lipid accumulation in hepatic cells. However, it has yet to be determined whether other HCV proteins are associated with lipid metabolism. The NS5A augmented the transcriptional activity and gene expression of PPARgamma. Furthermore, NS5A increased the ability to recruit the transcriptional coactivator PGC-1s to the PPRE with PPARgamma, as well as the interaction with PPARgamma2 and PGC-1alpha. Our results indicate that NS5A may exploit multiple strategies that enhance PPARgamma-induced lipid accumulation.
脂肪变性是慢性丙型肝炎病例中疾病进展的既定危险因素。最近有研究表明，丙型肝炎病毒（HCV）核心蛋白和非结构（NS）2蛋白（NS2）可诱导肝细胞中的脂质积累。然而，其他HCV蛋白是否与脂质代谢有关尚待确定。NS5A增强了PPARγ的转录活性和基因表达。此外，NS5A增强了与PPARγ一起将转录共激活因子PGC-1s招募至PPRE的能力，以及与PPARγ2和PGC-1α的相互作用。我们的结果表明，NS5A可能采用多种策略来增强PPARγ诱导的脂质积累。
