HCV E2 may induce apoptosis of Huh-7 cells via a mitochondrial-related caspase pathway
- School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan (China) and Department of Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan (China)
- Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan (China)
- Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan (China)
Introduction: One unusual characteristic of HCV is to establish chronic infection and the precise mechanisms remain unclear. Materials and methods: Huh-7 cells were transiently transfected with E2 and subjected to MTT assay, DNA fragmentation assay, and Western blotting to see the impact of E2 protein on apoptosis. Results and discussion: E2 may inhibit cell proliferation by inducing apoptosis and pro-caspases 3, 8, and 9 were cleaved and activated to result in the presence of active forms in a time-dependent fashion, which suggest that E2-induced apoptosis is caspase-dependent. Furthermore, the cytosolic level of cytochrome c was increased together with a gradually down-regulated Bcl-2 and up-regulated Bax protein expression. The continuing reduction of Bid protein and the gradual increase of tBid protein also indicated that a time-dependent increased turn-over of Bid protein into tBid. Taken together, our data suggested that HCV E2 may induce apoptosis through a mitochondrial damage-mediated caspase pathway.
- OSTI ID:
- 20854320
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 345, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2006.04.118; PII: S0006-291X(06)00961-2; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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