Abstract:
:Previous studies indicated that hepatitis C virus core protein influences cellular apoptosis. However, the precise mechanisms of the effects are not fully understood. Therefore, in this study, we examined the mechanisms of the effects on cell apoptosis by core protein, using transiently transfected and magnetically collected core-producing HepG2 cells. First, to elucidate the target site of core protein in the apoptotic pathway, we examined the activation of caspases after anti-Fas antibody stimulation. Core protein inhibited the apoptotic cascade downstream from caspase 8 and upstream from caspase 3. Next, to clarify more direct mechanisms of this effect, mRNA levels of several bcl-2-related genes were examined. An RNase protection assay showed that the mRNA of bcl-xl increased in the core-producing cells. We showed that this increase was mediated by the enhancement of bcl-x promoter activity by core protein through an extracellular-regulated kinase pathway. These results suggest that core protein inhibits apoptosis at the mitochondria level through augmentation of Bcl-x expression, resulting in an inhibition of caspase 3 activation.
journal_name
Virologyjournal_title
Virologyauthors
Otsuka M,Kato N,Taniguchi H,Yoshida H,Goto T,Shiratori Y,Omata Mdoi
10.1006/viro.2002.1371subject
Has Abstractpub_date
2002-04-25 00:00:00pages
84-93issue
1eissn
0042-6822issn
1096-0341pii
S0042682202913711journal_volume
296pub_type
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