Brief Article
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World J Gastroenterol. Apr 14, 2013; 19(14): 2262-2269
Published online Apr 14, 2013. doi: 10.3748/wjg.v19.i14.2262
Hepatitis B virus induces expression of cholesterol metabolism-related genes via TLR2 in HepG2 cells
Ying-Ju Li, Ping Zhu, Yu Liang, Wei-Guo Yin, Jian-Hua Xiao
Ying-Ju Li, Yu Liang, Wei-Guo Yin, Jian-Hua Xiao, Institute of Pathogenic Biology, University of South China, Hengyang 421001, Hunan Province, China
Ying-Ju Li, Department of Infectious Diseases, the First Affiliated Hospital of University of South China, Hengyang 421001, Hunan Province, China
Ping Zhu, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, Guangdong Province, China
Author contributions: Li YJ and Zhu P contributed equally to this work; Li YJ, Zhu P and Xiao JH designed the research; Li YJ, Liang Y and Yin WG performed the research; Li YJ and Xiao JH wrote the paper.
Supported by The Youth Foundation of Hunan Provincial Education Department, No. 11B110; the Graduate Innovation Project of Hunan Provincial Education Department, No. CX2010B382
Correspondence to: Jian-Hua Xiao, Professor, Institute of Pathogenic Biology, University of South China, Hengyang 421001, Hunan Province, China. jhxiao223@163.com
Telephone: +86-734-8282232 Fax: +86-734-8282232
Received: November 9, 2012
Revised: March 1, 2013
Accepted: March 8, 2013
Published online: April 14, 2013
Processing time: 156 Days and 7.8 Hours
Abstract

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.

Keywords: Hepatitis B virus; Toll-like receptors; Low-density lipoprotein receptor; 3-hydroxy-3-methylglutharyl-coenzyme A reductase

Core tip: This study investigated whether hepatitis B virus (HBV) exacerbates hepatic cholesterol accumulation and explored the underlying mechanisms. The authors found that adenovirus HBV increased low-density lipoprotein receptor and 3-hydroxy-3-methylglutharyl-coenzyme A reductase expression, resulting in exacerbated cholesterol accumulation in HepG2 cells, which was mediated via the toll-like receptor 2 pathway. These results may also have implications in the treatment of atherosclerosis.