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
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資料タイプ |
学術雑誌論文
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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.
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掲載誌名 |
Ecotoxicology and Environmental Safety
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ISSN | 01476513
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cat書誌ID | AA00179452
AA1154269X
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出版者 | Elsevier
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巻 | 222
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開始ページ | 112531
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発行日 | 2021-07-21
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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/).
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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
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著者版フラグ |
出版社版
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部局 |
歯学系
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