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Radiation induces apoptosis through endogenous Tumor Necrosis Factor alpha via activation of MEK/p38 MAPK and mitochondria/caspases pathways in Jurkat T leukemia cells
https://repo.qst.go.jp/records/69247
https://repo.qst.go.jp/records/69247d0d81507-2d7e-48c6-9120-542e53d330c6
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2007-12-26 | |||||
| タイトル | ||||||
| タイトル | Radiation induces apoptosis through endogenous Tumor Necrosis Factor alpha via activation of MEK/p38 MAPK and mitochondria/caspases pathways in Jurkat T leukemia cells | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Sudo, Makoto
× Sudo, Makoto× Sai, Sei× Akashi, Makoto× 須藤 誠× 崔 星× 明石 真言 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Tumor necrosis factor alpha (TNFalpha) is one of mediators of apoptosis as well as inflammation and immunity, and is produced upon radiation exposure. TNFalpha is a unique proinflammatory cytokine whose signaling pathways are linked to both anti- and pro-apoptotic responses in many cell types. To better understand the role of TNFalpha after high dose radiation, we have knocked-down TNFalpha by siRNA and examined changes of apoptosis-related proteins in human Jurkat T leukemia cells. Jurkat cells were transfected with TNFalpha-specific siRNA. Both control and TNFalpha-siRNA transfected cells were pretreated with an inhibitor of MEK, p38 MAPK or PI3K, and were irradiated with X-ray at a dose of 10Gy. DNA fragmentation analysis showed that transfection with TNFalpha- siRNA significantly blocked radiation-induced apoptosis. Western blot analysis showed that radiation induced phosphorylation of both ERK and p38 MAPK, which was further enhanced in TNFalpha- siRNA transfected cells even in the presence of a specific inhibitor of MEK or p38 MAPK. Phosphorylation of Akt was also induced in TNFalpha-siRNA transfected cells after irradiation. Radiation induced Bax expression and caspase-3 activation in the control cells, and transfection with TNFalpha-siRNA suppressed caspase-3 activation and up-regulated expression of Bcl-2 and Bcl-xL, whereas further enhanced Bax expression was observed. In conclusion, radiation induces apoptosis through activation of MEK/p38 MAPK and caspase/mitochondria pathways requiring TNFalpha. Further studies on the mechanisms are in progress. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 第30回日本分子生物学会年会･第80回日本生化学会大会合同大会 | |||||
| 発表年月日 | ||||||
| 日付 | 2007-12-15 | |||||
| 日付タイプ | Issued | |||||
