Document Detail

Premature cell cycle entry induced by hepatitis B virus regulatory HBx protein during compensatory liver regeneration.
MedLine Citation:
PMID:  19074903     Owner:  NLM     Status:  MEDLINE    
The cycles of cell death and compensatory regeneration that occur during chronic hepatitis B virus (HBV) infection are central to viral pathogenesis and are a risk factor for the development of liver cancer. The HBV genome encodes one regulatory protein, HBx, which is required for virus replication, although its precise role in replication and pathogenesis is unclear. Because HBx can induce the G(0)-G(1) transition in cultured cells, the purpose of this study was to examine the effect of HBx during liver regeneration. Transgenic mice expressing HBx (ATX) and their wild-type (WT) littermates were used in the partial hepatectomy (PH) model for compensatory regeneration. Liver tissues collected from ATX and WT mice at varying sacrifice time points after PH were examined for markers of cell cycle progression. When compared with WT liver tissues, ATX livers had evidence of premature cell cycle entry as assessed by several variables (BrdUrd incorporation, proliferating cell nuclear antigen and mitotic indices, and reduced steady-state p21 protein levels). However, HBx did not affect apoptosis, glycogen storage, or PH-induced steatosis. Together, these results show that HBx expression can induce cell cycle progression within the regenerating liver. Our data are consistent with a model in which HBx expression contributes to liver disease and cancer formation by affecting early steps in liver regeneration.
Amanda J Hodgson; Victor V Keasler; Betty L Slagle
Related Documents :
2384443 - Morpho-functional characterization of cultured pigment cells from rana esculenta l. liver.
7955093 - Cell proliferation and cell death (apoptosis) in hepatic preneoplasia and neoplasia are...
21103883 - Differentiation- and polarization-dependent zinc tolerance in caco-2 cells.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cancer research     Volume:  68     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-12-16     Completed Date:  2009-01-15     Revised Date:  2013-06-04    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10341-8     Citation Subset:  IM    
Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cell Cycle / physiology
Cell Division / physiology
DNA / biosynthesis
Hepatitis B, Chronic / metabolism,  pathology
Hepatocytes / cytology,  physiology
Liver Regeneration / physiology*
Mice, Transgenic
Multienzyme Complexes / genetics
Phosphodiesterase I / genetics
Phosphoric Diester Hydrolases
Pyrophosphatases / genetics
Viral Regulatory and Accessory Proteins / biosynthesis,  genetics,  physiology*
Grant Support
CA095388/CA/NCI NIH HHS; R01 CA095388-05/CA/NCI NIH HHS
Reg. No./Substance:
0/Multienzyme Complexes; 0/Trans-Activators; 0/Viral Regulatory and Accessory Proteins; 0/hepatitis B virus X protein; 9007-49-2/DNA; EC 3.1.4.-/Phosphoric Diester Hydrolases; EC I; EC phosphodiesterase; EC 3.6.1.-/Pyrophosphatases

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

Previous Document:  Genome-wide Allelic State Analysis on Flow-Sorted Tumor Fractions Provides an Accurate Measure of Ch...
Next Document:  250K single nucleotide polymorphism array karyotyping identifies acquired uniparental disomy and hom...