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  1. 30 医学部・医学研究科・保健学研究科
  2. 30a 学術雑誌論文
  3. 1.学術雑誌論文

Involvement of reactive oxygen species in ionizing radiation-induced upregulation of cell surface Toll-like receptor 2 and 4 expression in human monocytic cells

http://hdl.handle.net/10129/00006523
http://hdl.handle.net/10129/00006523
d7494653-56b4-4db4-a98b-bdb45262f721
名前 / ファイル ライセンス アクション
rrx011.pdf rrx011 (896.4 kB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2019-03-05
タイトル
タイトル Involvement of reactive oxygen species in ionizing radiation-induced upregulation of cell surface Toll-like receptor 2 and 4 expression in human monocytic 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_6501
資源タイプ journal article
著者 Yoshino, Hironori

× Yoshino, Hironori

Yoshino, Hironori

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Kashiwakura, Ikuo

× Kashiwakura, Ikuo

Kashiwakura, Ikuo

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著者所属
値 Hirosaki Univ, Grad Sch Hlth Sci, Dept Radiat Sci
抄録
内容記述タイプ Abstract
内容記述 Toll-like receptors (TLRs) are pattern recognition receptors that recognize pathogen-associated molecular patterns and are indispensable for antibacterial and antiviral immunity. Our previous report showed that ionizing radiation increases the cell surface expressions of TLR2 and TLR4 and enhances their responses to agonists in human monocytic THP1 cells. The present study investigated how ionizing radiation increases the cell surface expressions of TLR2 and TLR4 in THP1 cells. The THP1 cells treated or not treated with pharmaceutical agents such as cycloheximide and N-acetyl-L-cysteine (NAC) were exposed to X-ray irradiation, following which the expressions of TLRs and mitogen-activated protein kinase were analyzed. X-ray irradiation increased the mRNA expressions of TLR2 and TLR4, and treatment with a protein synthesis inhibitor cycloheximide abolished the radiation-induced upregulation of their cell surface expressions. These results indicate that radiation increased those receptors through de novo protein synthesis. Furthermore, treatment with an antioxidant NAC suppressed not only the radiation-induced upregulation of cell surface expressions of TLR2 and TLR4, but also the radiation-induced activation of the c-Jun N-terminal kinase (JNK) pathway. Since it has been shown that the inhibitor for JNK can suppress the radiation-induced upregulation of TLR expression, the present results suggest that ionizing radiation increased the cell surface expressions of TLR2 and TLR4 through reactive oxygen species-mediated JNK activation.
書誌情報 JOURNAL OF RADIATION RESEARCH

巻 58, 号 5, p. 626-635, 発行日 2017-09
ISSN
収録物識別子タイプ ISSN
収録物識別子 0449-3060
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 10.1093/jrr/rrx011
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
資源タイプ
値 Article
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