Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-7-24
pubmed:abstractText
Human hepatitis B virus X protein (HBx) is associated with the induction of oxidative stress, which is considered significant in the development of liver damage. In this study, we investigated the molecular mechanisms by which HBx induced lipid peroxidation and tumor necrosis factor-alpha (TNF-alpha) expression through regulation of selenoprotein P (SeP) expression in the human hepatoma cell line, HepG2. Forced expression of HBx significantly down-regulated the expression of SeP mRNA and protein in both the cell lysates and the culture medium. Lipid peroxidation increased 2.5-fold when expression of the SeP protein was blocked with a SeP antisense vector. Also, HBx transfection increased lipid peroxidation by 3.0-fold, whereas the hepatitis B virus core protein (HBc) had no significant effects. The induction of lipid peroxidation due to the block in SeP protein expression or treatment with ferric chloride (FeCl(3)) up-regulated the expression levels of TNF-alpha mRNA and protein. The pattern of HBx-induced lipid peroxidation and TNF-alpha up-regulation was reversed by SeP introduction. These results suggest that HBx induces lipid peroxidation via down-regulation of SeP expression, resulting in increased expression of TNF-alpha in the human hepatoma cell line, HepG2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
1638
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-56
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Hepatitis B virus X protein induces TNF-alpha expression via down-regulation of selenoprotein P in human hepatoma cell line, HepG2.
pubmed:affiliation
School of Biological Sciences, Seoul National University, 151-742, Seoul, South Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't