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The green tea component (-)-epigallocatechin-3-gallate sensitizes primary endothelial cells to Arsenite-induced apoptosis by decreasing C-Jun n-Terminal Kinase-mediated Catalase activity

Title
The green tea component (-)-epigallocatechin-3-gallate sensitizes primary endothelial cells to Arsenite-induced apoptosis by decreasing C-Jun n-Terminal Kinase-mediated Catalase activity
Authors
KimJ.-Y.ChoiLeeH.-J.ByunC.J.ParkJ.-H.J.H.ChoH.-S.S.-J.JoS.A.I.
Ewha Authors
조인호
SCOPUS Author ID
조인호scopus
Issue Date
2015
Journal Title
PLoS ONE
ISSN
1932-6203JCR Link
Citation
vol. 10, no. 9
Publisher
Public Library of Science
Indexed
SCIE; SCOPUS WOS scopus
Abstract
The green tea component (-)-epigallocatechin-3-gallate (EGCG) has been shown to sensitize many different types of cancer cells to anticancer drug-induced apoptosis, although it protects against non-cancerous primary cells against toxicity from certain conditions such as exposure to arsenic (As) or ultraviolet irradiation. Here, we found that EGCG promotes As-induced toxicity of primary-cultured bovine aortic endothelial cells (BAEC) at doses in which treatment with each chemical alone had no such effect. Increased cell toxicity was accompanied by an increased condensed chromatin pattern and fragmented nuclei, cleaved poly(ADP-ribose) polymerase (PARP), activity of the pro-Apoptotic enzymes caspases 3, 8 and 9, and Bax translocation into mitochondria, suggesting the involvement of an apoptotic signaling pathway. Fluorescence activated cell sorting analysis revealed that compared with EGCG or As alone, combined EGCG and As (EGCG/As) treatment significantly induced production of reactive oxygen species (ROS), which was accompanied by decreased catalase activity and increased lipid peroxidation. Pretreatment with N-Acetyl-Lcysteine or catalase reversed EGCG/As-induced caspase activation and EC toxicity. EGCG/As also increased the phosphorylation of c-Jun N-Terminal kinase (JNK), which was not reversed by catalase. However, pretreatment with the JNK inhibitor SP600125 reversed all of the observed effects of EGCG/As, suggesting that JNK may be the most upstream protein examined in this study. Finally, we also found that all the observed effects by EGCG/As are true for other types of EC tested. In conclusion, this is firstly to show that EGCGsensitizes non-cancerous EC to As-induced toxicity through ROS-mediated apoptosis, which was attributed at least in part to a JNK-Activated decrease in catalase activity. Copyright: © 2015 Kim et al.
DOI
10.1371/journal.pone.0138590
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의학전문대학원 > 의학과 > Journal papers
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