Hepatitis B virus induces expression of cholesterol metabolism-related genes via TLR2 in HepG2 cells  

作　　者：Ying-Ju Li Ping Zhu Yu Liang Wei-Guo Yin Jian-Hua Xiao 

机构地区：[1]Institute of Pathogenic Biology,University of South China [2]Department of Infectious Diseases,the First Affiliated Hospital of University of South China [3]Guangdong Cardiovascular Institute,Guangdong General Hospital,Guangdong Academy of Medical Sciences

出　　处：《World Journal of Gastroenterology》2013年第14期2262-2269,共8页世界胃肠病学杂志（英文版）

基　　金：Supported by The Youth Foundation of Hunan Provincial Education Department,No.11B110;the Graduate Innovation Project of Hunan Provincial Education Department,No.CX2010B382

摘　　要：AIM:To investigate whether hepatitis B virus(HBV) exacerbates hepatic cholesterol accumulation,and explore the underlying mechanisms.METHODS:HepG2 cells were infected with adenovirus(Ad) containing 1.3-fold overlength HBV genome.Realtime polymerase chain reaction and Western blotting were used to measure mRNA and protein expression of target genes.Cholesterol accumulation was measured by fluorescence microscopy.Cell toxicity due to Ad-HBV treatment was determined by the mitochondrial tetrazolium assay.The protein levels of toll-like receptors(TLRs) were determined by Western blotting.RESULTS:Ad-HBV increased hepatic cholesterol accumulation and enhanced the mRNA and protein levels oflow-density lipoprotein receptor(LDLR) and 3-hydroxy3-methylglutharyl-coenzyme A reductase(HMGCoAr) mRNA and protein expression in HepG2 cells.In addition,these inductive effects were partly offset by suppressing TLR2 expression levels by small interfering RNA in HepG2 cells.CONCLUSION:Ad-HBV increases LDLR and HMGCoAr expression,resulting in exacerbated cholesterol accumulation in HepG2 cells,which was mediated via the TLR2 pathway.AIM: To investigate whether hepatitis B virus (HBV) exacerbates hepatic cholesterol accumulation, and explore the underlying mechanisms. METHODS: HepG2 cells were infected with adenovirus (Ad) containing 1.3-fold overlength HBV genome. Real-time polymerase chain reaction and Western blotting were used to measure mRNA and protein expression of target genes. Cholesterol accumulation was measured by fluorescence microscopy. Cell toxicity due to Ad-HBV treatment was determined by the mitochondrial tetrazolium assay. The protein levels of toll-like receptors (TLRs) were determined by Western blotting. RESULTS: Ad-HBV increased hepatic cholesterol accumulation and enhanced the mRNA and protein levels of low-density lipoprotein receptor (LDLR) and 3-hydroxy-3-methylglutharyl-coenzyme A reductase (HMGCoAr) mRNA and protein expression in HepG2 cells. In addition, these inductive effects were partly offset by suppressing TLR2 expression levels by small interfering RNA in HepG2 cells. CONCLUSION: Ad-HBV increases LDLR and HMGCoAr expression, resulting in exacerbated cholesterol accumulation in HepG2 cells, which was mediated via the TLR2 pathway.

关 键 词：Hepatitis B virus TOLL-LIKE receptors Lowdensity LIPOPROTEIN receptor 3-hydroxy-3-methylglutharyl-coenzyme A REDUCTASE 

分 类 号：R512.62[医药卫生—内科学]