Increased Proinflammatory Cytokine Production and Decreased Cholesterol Efflux Due to Downregulation of ABCG1 in Macrophages Exposed to Indoxyl Sulfate.

• Material Type: 博士論文
• Title: Increased Proinflammatory Cytokine Production and Decreased Cholesterol Efflux Due to Downregulation of ABCG1 in Macrophages Exposed to Indoxyl Sulfate.
• Author/Editor: Matsuo, Koji
• Publication, Distribution, etc.: 新潟大学
• Publication Date: 2016-03-23
• Publication Date (W3CDTF): 2016-03-23
• Alternative Title: Increased Proinflammatory Cytokine Production and Decreased Cholesterol Efflux Due to Downregulation of ABCG1 in Macrophages Exposed to Indoxyl Sulfate.; インドキシル硫酸はマクロファージの炎症反応を促進し、ABCG1を減少させることにより脂質引き抜き能を低下させる
• Degree Grantor: 新潟大学
• Date Granted: 2016-03-23
• Date Granted (W3CDTF): 2016-03-23
• Dissertation Number: 甲第4124号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第4124号
• Text Language Code: eng
• Subject Heading: indoxyl sulfate; macrophage; chronic kidney disease; atherosclerosis
• Note (General): One of the possible causes of enhanced atherosclerosis in patients with chronic kidney disease (CKD) is the accumulation of uremic toxins. Since macrophage foam cell formation is a hallmark of atherosclerosis, we examined the direct effect of indoxyl sulfate (IS), a representative uremic toxin, on macrophage function. Macrophages differentiated from THP-1 cells were exposed to IS in vitro. IS decreased the cell viability of THP-1 derived macrophages but promoted the production of inflammatory cytokines (IL-1β, IS 1.0 mM: 101.8 ± 21.8 pg/mL vs. 0 mM: 7.0 ± 0.3 pg/mL, TNF-α, IS 1.0 mM: 96.6 ± 11.0 pg/mL vs. 0 mM: 15.1 ± 3.1 pg/mL) and reactive oxygen species. IS reduced macrophage cholesterol efflux (IS 0.5 mM: 30.3% ± 7.3% vs. 0 mM: 43.5% ± 1.6%) and decreased ATP-binding cassette transporter G1 expression. However, lipid uptake into cells was not enhanced. A liver X receptor (LXR) agonist, T0901317, improved IS-induced production of inflammatory cytokines as well as reduced cholesterol efflux. In conclusion, IS induced inflammatory reactions and reduced cholesterol efflux in macrophages. Both effects of IS were improved with activation of LXR. Direct interactions of uremic toxins with macrophages may be a major cause of atherosclerosis acceleration in patients with CKD.; 学位の種類: 博士（医学）. 報告番号: 甲第4124号. 学位記番号: 新大院博（医）甲第691号. 学位授与年月日: 平成28年3月23日; Toxins. 2015, 7(8), 3155-3166.; 新大院博（医）甲第691号; 元資料の権利情報 : Copyright(C) 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/)
• DOI: info:doi/10.3390/toxins7083155; https://doi.org/info:doi/10.3390/toxins7083155
• Persistent ID (NDL): info:ndljp/pid/9984819; https://dl.ndl.go.jp/pid/9984819
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2016-06-03T01:05:16+09:00
• Date Created (W3CDTF): 2019-08-05
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
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• Periodical Title (URI): http://hdl.handle.net/10191/41923
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp