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

doi:https://doi.org/10.1016/j.bbrc.2006.04.118

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

Full Record
Other Related Research

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:

Chiou, H -L ^[1]; Hsieh, Y -S ^[2]; Hsieh, M -R ^[2]; Chen, T -Y ^[3]

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)

Publication Date:: 2006-06-23

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.

Copy to clipboard


                    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

Copy to clipboard


                    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.

Copy to clipboard


                    
@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}

}

Copy to clipboard

Journal Article:

https://doi.org/10.1016/j.bbrc.2006.04.118

Other availability

Find in Google Scholar

Search WorldCat to find libraries that may hold this journal

Save / Share:

Export Metadata

Save to My Library

Similar records in OSTI.GOV collections:

Ofloxacin induces apoptosis in microencapsulated juvenile rabbit chondrocytes by caspase-8-dependent mitochondrial pathway

Journal Article Zhiguo, Sheng ; Xiaojuan, Cao ; Peng Shuangqing ; ... - Toxicology and Applied Pharmacology

Quinolones (QNs)-induced arthropathy is an important toxic effect in immature animals leading to restriction of their therapeutic use in pediatrics. However, the exact mechanism still remains unclear. Recently, we have demonstrated that ofloxacin, a typical QN, induces apoptosis of alginate microencapsulated juvenile rabbit joint chondrocytes by disturbing the {beta}{sub 1} integrin functions and inactivating the ERK/MAPK signaling pathway. In this study, we extend our initial observations to further elucidate the mechanism(s) of ofloxacin-induced apoptosis by utilizing specific caspase inhibitors. Pretreatment with both caspase-9-specific inhibitor zLEHD-fmk and caspase-8 inhibitor zIETD-fmk attenuated ofloxacin-induced apoptosis and activation of caspase-3 of chondrocyte in amore »« less
https://doi.org/10.1016/j.taap.2007.08.025
miR-138 protects cardiomyocytes from hypoxia-induced apoptosis via MLK3/JNK/c-jun pathway

Journal Article He, Siyi ; Liu, Peng ; Jian, Zhao ; ... - Biochemical and Biophysical Research Communications

Highlights: •First time to find miR-138 is up-regulated in hypoxic cardiomyocytes. •First time to find miR-138 targets MLK3 and regulates JNK/c-jun pathway. •Rare myocardial biopsy of patients with CHD were collected. •Both silence and overexpression of miR-138 were implemented. •Various methods were used to detect cell function. -- Abstract: Cardiomyocytes experience a series of complex endogenous regulatory mechanisms against apoptosis induced by chronic hypoxia. MicroRNAs are a class of endogenous small non-coding RNAs that regulate cellular pathophysiological processes. Recently, microRNA-138 (miR-138) has been found related to hypoxia, and beneficial for cell proliferation. Therefore, we intend to study the role ofmore »« less
https://doi.org/10.1016/J.BBRC.2013.10.151
atRA-induced apoptosis of mouse embryonic palate mesenchymal cells involves activation of MAPK pathway

Journal Article Zengli, Yu ; Ying, Xing - Toxicology and Applied Pharmacology

Our previous studies have shown that atRA treatment resulted in cell-cycle block and growth inhibition in mouse embryonic palatal mesenchymal (MEPM). In the current study, gestation day (GD) 13 MEPM cells were used to test the hypothesis that the growth inhibition by atRA is due to apoptosis. The effects of atRA on apoptosis were assessed by performing MTT assay, Cell Death Detection ELISA and flow cytometry, respectively. Data analysis confirmed that atRA treatment induced apoptosis-like cell death, as shown by decreased cell viability and increased fragmented DNA and sub-G1 fraction. atRA-induced apoptosis was associated with upregulation of bcl-2, translocation ofmore »« less
Trichodermin induces cell apoptosis through mitochondrial dysfunction and endoplasmic reticulum stress in human chondrosarcoma cells

Journal Article Su, Chen-Ming ; Wang, Shih-Wei ; Lee, Tzong-Huei ; ... - Toxicology and Applied Pharmacology

Chondrosarcoma is the second most common primary bone tumor, and it responds poorly to both chemotherapy and radiation treatment. Nalanthamala psidii was described originally as Myxosporium in 1926. This is the first study to investigate the anti-tumor activity of trichodermin (trichothec-9-en-4-ol, 12,13-epoxy-, acetate), an endophytic fungal metabolite from N. psidii against human chondrosarcoma cells. We demonstrated that trichodermin induced cell apoptosis in human chondrosarcoma cell lines (JJ012 and SW1353 cells) instead of primary chondrocytes. In addition, trichodermin triggered endoplasmic reticulum (ER) stress protein levels of IRE1, p-PERK, GRP78, and GRP94, which were characterized by changes in cytosolic calcium levels. Furthermore,more »« less
https://doi.org/10.1016/J.TAAP.2013.06.010
N,N-dimethyl phytosphingosine induces caspase-8-dependent cytochrome c release and apoptosis through ROS generation in human leukemia cells

Journal Article Kim, Byeong Mo ; Choi, Yun Jung ; Han, Youngsoo ; ... - Toxicology and Applied Pharmacology

N,N-dimethyl phytosphingosine (DMPS) blocks the conversion of sphingosine to sphingosine-1-phosphate (S1P) by the enzyme sphingosine kinase (SK). In this study, we elucidated the apoptotic mechanisms of DMPS action on a human leukemia cell line using functional pharmacologic and genetic approaches. First, we demonstrated that DMPS-induced apoptosis is evidenced by nuclear morphological change, distinct internucleosomal DNA fragmentation, and an increased sub-G1 cell population. DMPS treatment led to the activation of caspase-9 and caspase-3, accompanied by the cleavage of poly(ADP-ribose) polymerase (PARP) and led to cytochrome c release, depolarization of the mitochondrial membrane potential, and downregulation of the anti-apoptotic members of themore »« less
https://doi.org/10.1016/j.taap.2009.05.020

Similar Records