| Item type |
デフォルトアイテムタイプ_（フル）(1) |
| 公開日 |
2023-03-18 |
| タイトル |
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|
タイトル |
Dual Role of Superoxide Dismutase 2 Induced in Activated Microglia: OXIDATIVE STRESS TOLERANCE AND CONVERGENCE OF INFLAMMATORY RESPONSES |
|
言語 |
en |
| 作成者 |
Ishihara, Yasuhiro
Itoh, Kouichi
Ishida, Atsuhiko
Yamazaki, Takeshi
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| アクセス権 |
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アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 権利情報 |
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権利情報 |
This research was originally published in the Journal of Biological Chemistry. Yasuhiro Ishihara, Takuya Takemoto, Kouichi Itoh, Atsuhiko Ishida, and Takeshi Yamazaki. Dual Role of Superoxide Dismutase 2 Induced in Activated Microglia: OXIDATIVE STRESS TOLERANCE AND CONVERGENCE OF INFLAMMATORY RESPONSES. J. Biol. Chem. 2015; 290(37):22805-22817. © the American Society for Biochemistry and Molecular Biology. |
| 内容記述 |
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内容記述 |
Microglia are activated quickly in response to external pathogens or cell debris and clear these substances via the inflammatory response. However, excessive activation of microglia can be harmful to host cells due to the increased production of reactive oxygen species and proinflammatory cytokines. Superoxide dismutase 2 (SOD2) is reportedly induced under various inflammatory conditions in the central nervous system. We herein demonstrated that activated microglia strongly express SOD2 and examined the role of SOD2, focusing on regulation of the microglial activity and the susceptibility of microglia to oxidative stress. When rat primary microglia were treated with LPS, poly(I:C), peptidoglycan, or CpG oligodeoxynucleotide, respectively, the mRNA and protein levels of SOD2 largely increased. However, an increased expression of SOD2 was not detected in the primary neurons or astrocytes, indicating that SOD2 is specifically induced in microglia under inflammatory conditions. The activated microglia showed high tolerance to oxidative stress, whereas SOD2 knockdown conferred vulnerability to oxidative stress. Interestingly, the production of proinflammatory cytokines was increased in the activated microglia treated with SOD2 siRNA compared with that observed in the control siRNA-treated cells. Pretreatment with NADPH oxidase inhibitors, diphenylene iodonium and apocynin, decreased in not only reactive oxygen species generation but also the proinflammatory cytokine expression. Notably, SOD2 knockdown largely potentiated the nuclear factor κB activity in the activated microglia. Taken together, increased SOD2 conferred tolerance to oxidative stress in the microglia and decreased proinflammatory cytokine production by attenuating the nuclear factor κB activity. Therefore, SOD2 might regulate neuroinflammation by controlling the microglial activities. |
|
言語 |
en |
| 内容記述 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
This work was supported in part by KAKENHI Grants 26740024, 30291149, and 22310041 from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (to Y. I., K. I., and T. Y.); a grant from the Fujii Foundation (to Y. I.); and a grant from the Hiroshima University Education and Research Support Foundation (to Y. I.). |
| 出版者 |
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出版者 |
The American Society for Biochemistry and Molecular Biology, Inc. |
| 言語 |
|
|
言語 |
eng |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 関連情報 |
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|
識別子タイプ |
DOI |
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|
関連識別子 |
10.1074/jbc.M115.659151 |
| 関連情報 |
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1074/jbc.M115.659151 |
| 収録物識別子 |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0021-9258 |
| 収録物識別子 |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
1083-351X |
| 開始ページ |
|
|
開始ページ |
22805 |
| 書誌情報 |
Journal of Biological Chemistry
Journal of Biological Chemistry
巻 290,
号 37,
p. 22805-22817,
発行日 2015-09-11
|
| 旧ID |
48598 |
J. Biol. Chem._290_22805.pdf (2.6 MB)
