論文

査読有り
2012年2月

RAGE mediates vascular injury and inflammation after global cerebral ischemia

NEUROCHEMISTRY INTERNATIONAL
  • Tomoya Kamide
  • ,
  • Yasuko Kitao
  • ,
  • Toshiaki Takeichi
  • ,
  • Akiko Okada
  • ,
  • Hiromi Mohri
  • ,
  • Ann Marie Schmidt
  • ,
  • Takayuki Kawano
  • ,
  • Seiichi Munesue
  • ,
  • Yasuhiko Yamamoto
  • ,
  • Hiroshi Yamamoto
  • ,
  • Jun-ichiro Hamada
  • ,
  • Osamu Hori

60
3
開始ページ
220
終了ページ
228
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.neuint.2011.12.008
出版者・発行元
PERGAMON-ELSEVIER SCIENCE LTD

The receptor for advanced glycation end products (RAGE) is a multi-ligand receptor involved in a diverse range of pathological conditions. To analyze the roles of RAGE and its decoy receptor, endogenous secretory RAGE (esRAGE), in the global cerebral ischemia, three different mouse cohorts, wild-type, RAGE(-/-), and esRAGE transgenic (Tg) mice were subjected to bilateral common carotid artery occlusion (BCCAO). RT-PCR and immunohistochemical analysis revealed that expression of RAGE was induced in the vascular cells at 12 h, and then in the neurons and glia from 3 to 7 days in the hippocampus after BCCAO. The numbers of surviving neurons in the hippocampal CA1 region were significantly higher in RAGE(-/-) and esRAGE Tg mice than those in wild-type mice in the periods between 24 h and 7 days after BCCAO. Lower levels of 3-nitrotyrosine (3-NT) and higher levels of endothelial nitric oxide synthase (eNOS), together with enlarged vascular areas were observed in RAGE(-/-) and esRAGE Tg mice at 12 h after BCCAO. In the later periods, expressions of glia-derived inflammatory mediators TNF alpha and inducible nitric oxide synthase (iNOS) were reduced in RAGE(-/-) and esRAGE Tg mice. These results suggest that RAGE may contribute to delayed neuronal death after global cerebral ischemia by enhancing vascular injury and deleterious glia-mediated inflammation. (C) 2011 Elsevier Ltd. All rights reserved.

Web of Science ® 被引用回数 : 39

リンク情報
DOI
https://doi.org/10.1016/j.neuint.2011.12.008
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/22202666
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000301632500002&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.neuint.2011.12.008
  • ISSN : 0197-0186
  • PubMed ID : 22202666
  • Web of Science ID : WOS:000301632500002

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