Document Detail

Hepatitis B virus X protein promotes proliferation and upregulates TGF-beta1 and CTGF in human hepatic stellate cell line, LX-2.
MedLine Citation:
PMID:  19208517     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Chronic hepatitis B virus (HBV) infection is a major cause of liver fibrosis, but the mechanisms underlying HBV-related fibrogenesis are still unknown. Although the roles of HBV X protein (HBx) remain poorly understood, it is thought to play an important role in the regulation of cellular growth and hepatocarcinogenesis. The aim of this study was to determine the role of HBx in liver fibrogenesis by studying the effect of HBx on the proliferation and expression of fibrosis-related molecules in the human hepatic stellate cell line, LX-2. METHODS: We established an in vitro co-culture system with LX-2 cells and a stable QSG7701-HBx cell line which had been transfected with the HBx gene. 3H-TdR incorporation and flow cytometry were used to determine the effects of HBx on the proliferation of LX-2 cells. Alpha-smooth muscle actin (alpha-SMA), transforming growth factor-beta1 (TGF-beta1), transforming growth factor-beta receptor II (TGF-betaRII), and connective tissue growth factor (CTGF) in LX-2 cells were analyzed by Western blotting. In addition, the expression levels of collagen type I (ColI) from the co-cultured media were measured by ELISA. RESULTS: 3H-TdR incorporation increased significantly in LX-2 cells co-cultured with QSG7701-HBx cells compared to those cultured with QSG7701-pcDNA3 and QSG7701 (non-tumorigenic human liver cell line). Cell cycle results revealed that HBx accelerated the progression of G1 to S in LX-2 cells. The expressions of alpha-SMA, TGF-beta1, TGF-betaRII, CTGF and ColI were significantly increased in the co-cultures of LX-2 cells with stable QSG7701-HBx cells. CONCLUSION: These results suggest that HBx may facilitate liver fibrosis by promoting hepatic stellate cell proliferation and upregulating the expression of fibrosis-related molecules.
Guang-Hui Guo; De-Ming Tan; Ping-An Zhu; Fei Liu
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Hepatobiliary & pancreatic diseases international : HBPD INT     Volume:  8     ISSN:  1499-3872     ISO Abbreviation:  HBPD INT     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-11     Completed Date:  2009-05-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101151457     Medline TA:  Hepatobiliary Pancreat Dis Int     Country:  China    
Other Details:
Languages:  eng     Pagination:  59-64     Citation Subset:  IM    
Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha 410008, China.
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MeSH Terms
Actins / metabolism
Cell Division / drug effects
Cell Line
Coculture Techniques
Collagen Type I / metabolism
Connective Tissue Growth Factor / metabolism*
Flow Cytometry
Hepatic Stellate Cells* / metabolism,  pathology,  virology
Hepatitis B, Chronic / metabolism,  pathology*
Liver Cirrhosis / metabolism,  pathology,  virology*
Protein-Serine-Threonine Kinases / metabolism
Receptors, Transforming Growth Factor beta / metabolism
Trans-Activators / genetics*,  metabolism
Transforming Growth Factor beta1 / metabolism*
Up-Regulation / drug effects
Viral Regulatory and Accessory Proteins / genetics*,  metabolism
Reg. No./Substance:
0/Actins; 0/CTGF protein, human; 0/Collagen Type I; 0/Receptors, Transforming Growth Factor beta; 0/Trans-Activators; 0/Transforming Growth Factor beta1; 0/Viral Regulatory and Accessory Proteins; 0/hepatitis B virus X protein; 139568-91-5/Connective Tissue Growth Factor; EC Kinases; EC growth factor-beta type II receptor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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