DSpace Fukushima Medical University

福島県立医科大学学術成果リポジトリ = Fukushima Medical University Repository >
福島医学会 = The Fukushima Society of Medical Science >
Fukushima Journal of Medical Science >
Vol.65 (2019) >

このアイテムの引用には次の識別子を使用してください: http://ir.fmu.ac.jp/dspace/handle/123456789/1056

このアイテムのファイル:

ファイル 記述 サイズフォーマット
FksmJMedSci_65_p109.pdf7.3 MBAdobe PDFダウンロード
タイトル: Integral role of receptor for advanced glycation end products (RAGE) in nondiabetic atherosclerosis
著者: Uekita, Hironori
Ishibashi, Toshiyuki
Shiomi, Masashi
Koyama, Hidenori
Ohtsuka, Shukuko
Yamamoto, Hiroshi
Yamagishi, Shoichi
Inoue, Hiroyoshi
Itabe, Hiroyuki
Sugimoto, Koichi
Kamioka, Masashi
Ohkawara, Hiroshi
Wada, Ikuo
Yasuchika, Takeishi
学内所属: 循環器・血液内科学講座
細胞科学研究部門
誌名/書名: Fukushima Journal of Medical Science
巻: 65
号: 3
開始ページ: 109
終了ページ: 121
発行日: 2019年
抄録: An advanced glycation end products (AGE)/a receptor for AGE (RAGE) axis plays a central role in the pathogenesis of diabetic vascular remodeling. This study was conducted to clarify the role of RAGE in nondiabetic atherosclerosis. We used the aortic and coronary atherosclerotic lesions of Watanabe heritable hyperlipidemic (WHHL) rabbits prone to myocardial infarction (WHHLMI) at 1 to 14 months. Immunohistochemistry demonstrated the significant expression of RAGE as early as at 1 month with the stronger expression at 3 and 7 months, which was remarkably diminished at 14 months. RAGE expression was concordant with AGE accumulation. The major original sources of RAGE expression were macrophages and smooth muscle cells in addition to endothelial cells, and RAGE expression was distributed in the areas of phospholipid products, a component of oxidized LDL and nitrotyrosine. The concentrations of serum AGE did not alter significantly with aging. These findings suggested the expression of RAGE was induced by hyperlipidemia and oxidative stress independent of diabetes in WHHLMI rabbits. Additionally, our in vitro study showed that silencing of RAGE tended to attenuate oxidized-LDL-triggered PAI-1 expression in human cultured macrophages, as well as oxidized-LDL-induced tissue factor expression in peritoneal macrophages, suggesting a possible role of RAGE in prothrombogenic molecular regulation. In conclusion, the present study provides in vivo evidence that RAGE plays an integral role in the initiation and progression of nondiabetic atherosclerosis, suggesting that RAGE may be a novel target for treating not only diabetic but also nondiabetic vascular complications.
出版者: The Fukushima Society of Medical Science
出版者(異表記): 福島医学会
本文の言語: eng
このページのURI: http://ir.fmu.ac.jp/dspace/handle/123456789/1056
本文URL: http://ir.fmu.ac.jp/dspace/bitstream/123456789/1056/1/FksmJMedSci_65_p109.pdf
ISSN: 0016-2590
2185-4610
DOI: 10.5387/fms.2019-12
PubMed番号: 31915324
関連ページ: https://doi.org/10.5387/fms.2019-12
権利情報: © 2019 The Fukushima Society of Medical Science. This article is licensed under a Creative Commons [Attribution-NonCommercial-ShareAlike 4.0 International] license.
権利情報: https://creativecommons.org/licenses/by-nc-sa/4.0/
出現コレクション:Vol.65 (2019)

このアイテムのファイル:

ファイル 記述 サイズフォーマット
FksmJMedSci_65_p109.pdf7.3 MBAdobe PDFダウンロード

このリポジトリに保管されているアイテムは、他に指定されている場合を除き、著作権により保護されています。

 

DSpace Software Copyright © 2002-2006 MIT and Hewlett-Packard