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Title: HCV E2 may induce apoptosis of Huh-7 cells via a mitochondrial-related caspase pathway

Abstract

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.

Authors:
 [1];  [2];  [2];  [3]
  1. 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)
  2. Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan (China)
  3. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan (China)
Publication Date:
OSTI Identifier:
20854320
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 345; Journal 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); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; BORON CHLORIDES; CELL PROLIFERATION; DAMAGE; DNA; HEPATITIS; PROTEINS; TIME DEPENDENCE; VIRUSES

Citation Formats

Chiou, H -L, Hsieh, Y -S, Hsieh, M -R, Chen, T -Y, and Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan. HCV E2 may induce apoptosis of Huh-7 cells via a mitochondrial-related caspase pathway. United States: N. p., 2006. Web. doi:10.1016/j.bbrc.2006.04.118.
Chiou, H -L, Hsieh, Y -S, Hsieh, M -R, Chen, T -Y, & Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan. HCV E2 may induce apoptosis of Huh-7 cells via a mitochondrial-related caspase pathway. United States. https://doi.org/10.1016/j.bbrc.2006.04.118
Chiou, H -L, Hsieh, Y -S, Hsieh, M -R, Chen, T -Y, and Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan. Fri . "HCV E2 may induce apoptosis of Huh-7 cells via a mitochondrial-related caspase pathway". United States. https://doi.org/10.1016/j.bbrc.2006.04.118.
@article{osti_20854320,
title = {HCV E2 may induce apoptosis of Huh-7 cells via a mitochondrial-related caspase pathway},
author = {Chiou, H -L and Hsieh, Y -S and Hsieh, M -R and Chen, T -Y and Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan},
abstractNote = {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.},
doi = {10.1016/j.bbrc.2006.04.118},
url = {https://www.osti.gov/biblio/20854320}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 345,
place = {United States},
year = {2006},
month = {6}
}