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ROS enhance angiogenic properties via regulation of NRF2 in tumor endothelial cells

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この文献へのリンクには次のURLを使用してください:http://hdl.handle.net/2115/67123

タイトル: ROS enhance angiogenic properties via regulation of NRF2 in tumor endothelial cells
著者: Hojo, Takayuki 著作を一覧する
Maishi, Nako 著作を一覧する
Towfik, Alam Mohammad 著作を一覧する
Akiyama, Kosuke 著作を一覧する
Ohga, Noritaka 著作を一覧する
Shindoh, Masanobu 著作を一覧する
Hida, Yasuhiro 著作を一覧する
Minowa, Kazuyuki 著作を一覧する
Fujisawa, Toshiaki 著作を一覧する
Hida, Kyoko 著作を一覧する
キーワード: tumor angiogenesis
tumor endothelial cells
reactive oxygen species
biglycan
nuclear factor erythroid 2-related factor 2
発行日: 2017年 7月11日
出版者: Impact Journals
誌名: Oncotarget
巻: 8
号: 28
開始ページ: 45484
終了ページ: 45495
出版社 DOI: 10.18632/oncotarget.17567
抄録: Reactive oxygen species (ROS) are unstable molecules that activate oxidative stress. Because of the insufficient blood flow in tumors, the tumor microenvironment is often exposed to hypoxic condition and nutrient deprivation, which induces ROS accumulation. We isolated tumor endothelial cells (TECs) and found that they have various abnormalities, although the underlying mechanisms are not fully understood. Here we showed that ROS were accumulated in tumor blood vessels and ROS enhanced TEC migration with upregulation of several angiogenesis related gene expressions. It was also demonstrated that these genes were upregulated by regulation of Nuclear factor erythroid 2-related factor 2 (NRF2). Among these genes, we focused on Biglycan, a small leucine-rich proteoglycan. Inhibition of Toll-like receptors 2 and 4, known BIGLYCAN (BGN) receptors, cancelled the TEC motility stimulated by ROS. ROS inhibited NRF2 expression in TECs but not in NECs, and NRF2 inhibited phosphorylation of SMAD2/3, which activates transcription of BGN. These results indicated that ROS-induced BGN caused the pro-angiogenic phenotype in TECs via NRF2 dysregulation.
資料タイプ: article
URI: http://hdl.handle.net/2115/67123
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 樋田 京子

 

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