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ID 116727
著者
Tang, Jing Nantong University
Liu, Yingqi Nantong University
Yuan, Jiaming Nantong University
Wu, Li Nantong University
Yu, Shali Nantong University
Huang, Chunyan Suzhou Center for Disease Control and Prevention
Wei, Haiyan Nantong University
Chen, Gang Nantong University
キーワード
Arsenic trioxide
BCL-2
Apoptosis
p38 MAPK
Phosphorylation
NF-κB
資料タイプ
学術雑誌論文
抄録
Inorganic arsenic compounds are environmental toxicants that are widely distributed in air, water, and food. B-cell lymphoma 2 (BCL-2) is an oncogene having anti-apoptotic function. In this study, we clarify that BCL-2, as a pro-apoptotic factor, participates in As2O3-induced apoptosis in BEAS-2B cells. Specifically, As2O3 stimulated the expression of BCL-2 mRNA and protein in a dose-dependent manner which was highly accumulated in the nucleus of BEAS-2B cell together with chromatin condensation and DNA fragmentation during apoptosis. Mechanistically, the process described above is mediated through the NF-κB and p38 MAPK signaling pathways, which can be abated by corresponding inhibitors, such as BAY11–7082 and SB203580, respectively. Additionally, BAY11–7082, actinomycin D, and cycloheximide have inhibitory effects on As2O3-induced expression of BCL-2 mRNA and protein, and restore the cell viability of BEAS-2B cells. Suppression of BCL-2 protein activation by ABT-199 also restored viability of BEAS-2B cell in As2O3-induced apoptosis. Furthermore, As2O3 increased the level of BCL-2 phosphorylation. These results suggest that in BEAS-2B cells, As2O3-induced apoptosis is mainly dominated by BCL-2 upregulation, nuclear localization and phosphorylation. The study presented here provides a novel insight into the molecular mechanism of BCL-2-induced apoptosis.
掲載誌名
Ecotoxicology and Environmental Safety
ISSN
01476513
cat書誌ID
AA00179452
AA1154269X
出版者
Elsevier
222
開始ページ
112531
発行日
2021-07-21
権利情報
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
EDB ID
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
歯学系