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  1. 0 資料タイプ別
  2. 02 学位論文
  1. 250 大学院医歯学総合研究科(医)
  2. 60 博士学位論文
  3. 10 博士学位論文

Indoxyl Sulfate Promotes Macrophage IL-1β Production by Activating Aryl Hydrocarbon Receptor/NF-_K/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated

http://hdl.handle.net/10191/50778
http://hdl.handle.net/10191/50778
d2327622-db06-4991-8f42-324ab9fbec5f
名前 / ファイル ライセンス アクション
h30nmk835.pdf 本文 (3.2 MB)
h30nmk835_a.pdf 要旨 (539.8 kB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2018-11-29
タイトル
タイトル Indoxyl Sulfate Promotes Macrophage IL-1β Production by Activating Aryl Hydrocarbon Receptor/NF-_K/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated
タイトル
言語 en
タイトル Indoxyl Sulfate Promotes Macrophage IL-1β Production by Activating Aryl Hydrocarbon Receptor/NF-_K/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated
言語
言語 eng
キーワード
主題Scheme Other
主題 uremic toxins
キーワード
主題Scheme Other
主題 indoxyl sulfate
キーワード
主題Scheme Other
主題 macrophage
キーワード
主題Scheme Other
主題 aryl hydrocarbon receptor
キーワード
主題Scheme Other
主題 nuclear factor-_KB
キーワード
主題Scheme Other
主題 inflammasome
キーワード
主題Scheme Other
主題 atherosclerosis
キーワード
主題Scheme Other
主題 cardiovascular disease
資源タイプ
資源 http://purl.org/coar/resource_type/c_46ec
タイプ thesis
その他のタイトル
その他のタイトル インドキシル硫酸は、アリルハイドロカーボン受容体/NF-_K/MAPK経路の活性化を介してIL-1βの発現を亢進させるが、NLRP3インフラマソームを活性化しない。
著者 Wakamatsu, Takuya

× Wakamatsu, Takuya

WEKO 175081

Wakamatsu, Takuya

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著者別名
識別子 175082
識別子Scheme WEKO
姓名 若松, 拓也
抄録
内容記述タイプ Abstract
内容記述 In chronic kidney disease (CKD) patients, accumulation of uremic toxins is associated with cardiovascular risk and mortality. One of the hallmarks of kidney disease-related cardiovascular disease is intravascular macrophage inflammation, but the mechanism of the reaction with these toxins is not completely understood. Macrophages differentiated from THP-1 cells were exposed to indoxyl sulfate (IS), a representative uremic toxin, and changes in inflammatory cytokine production and intracellular signaling molecules including interleukin (IL)-1, aryl hydrocarbon receptor (AhR), nuclear factor (NF)-_K, and mitogen-activated protein kinase (MAPK) cascades as well as the NLRP3 inflammasome were quantified by real-time PCR, Western blot analysis, and enzyme-linked immunosorbent assay. IS induced macrophage pro-IL-1β mRNA expression, although mature IL-1 was only slightly increased. IS increased AhR and the AhR-related mRNA expression; this change was suppressed by administration of proteasome inhibitor. IS promoted phosphorylation of NF-_KB p65 and MAPK enzymes; the reaction and IL-1 expression were inhibited by BAY11-7082, an inhibitor of NF-_KB. In contrast, IS decreased NLRP3 and did not change ASC, pro-caspase 1, or caspase-1 activation. IS-inducing inflammation in macrophages results from accelerating AhR-NF-_KB/MAPK cascades, but the NLRP3 inflammasome was not activated. These reactions may restrict mature IL-1β production, which may explain sustained chronic inflammation in CKD patients.
内容記述
内容記述タイプ Other
内容記述 学位の種類: 博士(医学). 報告番号: 甲第4498号. 学位記番号: 新大院博(医)甲第835号. 学位授与年月日: 平成30年9月20日
内容記述
内容記述タイプ Other
内容記述 Toxins. 2018, 10, 124.
書誌情報 発行日 2018-09-20
出版者
出版者 新潟大学
DOI
識別子タイプ DOI
関連識別子 info:doi/10.3390/toxins10030124
著者版フラグ
値 ETD
学位名
学位名 博士(医学)
学位授与機関
学位授与機関名 新潟大学
学位授与年月日
学位授与年月日 2018-09-20
学位授与番号
学位授与番号 13101甲第4498号
学位記番号
内容記述タイプ Other
内容記述 新大院博(医)甲第835号
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