WEKO3
アイテム
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/10191/50778d2327622-db06-4991-8f42-324ab9fbec5f
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
本文 (3.2 MB)
|
|
|
|
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 | ||||||
| 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 | en | |||||
| 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 | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_46ec | |||||
| 資源タイプ | 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 |
|||||
| 著者別名 | ||||||
| 識別子Scheme | WEKO | |||||
| 識別子 | 175082 | |||||
| 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 | |||||
