Calcium Release from Endoplasmic Reticulum Involves Calmodulin-Mediated NADPH Oxidase-Derived Reactive Oxygen Species Production in Endothelial Cells 7

• 資料種別: 博士論文
• ISSN: 1422-0067
• タイトル: Calcium Release from Endoplasmic Reticulum Involves Calmodulin-Mediated NADPH Oxidase-Derived Reactive Oxygen Species Production in Endothelial Cells
• 巻次・部編番号: 20 7
• 著者・編者: 櫻田, 隆悟
• 著者標目: 櫻田, 隆悟
• 出版事項: MDPI
• 出版年月日等: 2019-04-02
• 出版年（W3CDTF）: 2019-04-02
• 並列タイトル等: 血管内皮細胞において小胞体からのカルシウム放出は、カルモジュリンを介したNADPHオキシダーゼ由来の活性酸素種の生成に関与する
• タイトル（掲載誌）: International journal of molecular sciences
• 授与機関名: 浜松医科大学
• 授与年月日: 2020-03-16
• 授与年月日（W3CDTF）: 2020-03-16
• 報告番号: 甲第833号
• 学位: 博士（医学）
• 博論授与番号: 甲第833号
• 本文の言語コード: eng
• 件名標目: NADPH oxidase; reactive oxygen species; endothelial cell; endoplasmic reticulum; calcium; calmodulin
• 対象利用者: 一般
• 一般注記: doctoral; 医学系研究科; Background: Previous studies demonstrated that calcium/calmodulin (Ca2+/CaM) activates nicotinamide adenine dinucleotide phosphate oxidases (NOX). In endothelial cells, the elevation of intracellular Ca2+ level consists of two components: Ca2+ mobilization from the endoplasmic reticulum (ER) and the subsequent store-operated Ca2+ entry. However, little is known about which component of Ca2+ increase is required to activate NOX in endothelial cells. Here, we investigated the mechanism that regulates NOX-derived reactive oxygen species (ROS) production via a Ca2+/CaM-dependent pathway.Methods: We measured ROS production using a fluorescent indicator in endothelial cells and performed phosphorylation assays.Results: Bradykinin (BK) increased NOX-derived cytosolic ROS. When cells were exposed to BK with either a nominal Ca2+-free or 1 mM of extracellular Ca2+ concentration modified Tyrode's solution, no difference in BK-induced ROS production was observed; however, chelating of cytosolic Ca2+ by BAPTA/AM or the depletion of ER Ca2+ contents by thapsigargin eliminated BK-induced ROS production. BK-induced ROS production was inhibited by a CaM inhibitor; however, a Ca2+/CaM-dependent protein kinase II (CaMKII) inhibitor did not affect BK-induced ROS production. Furthermore, BK stimulation did not increase phosphorylation of NOX2, NOX4, and NOX5.Conclusions: BK-induced NOX-derived ROS production was mediated via a Ca2+/CaM-dependent pathway; however, it was independent from NOX phosphorylation. This was strictly regulated by ER Ca2+ contents.
• DOI: info:doi/10.3390/ijms20071644; https://doi.org/info:doi/10.3390/ijms20071644
• 国立国会図書館永続的識別子: info:ndljp/pid/11498579; https://dl.ndl.go.jp/pid/11498579
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 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
• 収集根拠: 博士論文（自動収集）
• 受理日（W3CDTF）: 2020-06-07T00:39:19+09:00
• 作成日（W3CDTF）: 2020-04-30
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://hdl.handle.net/10271/00003728; https://hama-med.repo.nii.ac.jp/records/3596
• 連携機関・データベース: 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

目次

2023-12-06 再収集