論文

査読有り
2005年12月

Selective uptake and efflux of cholesteryl linoleate in LDL by macrophages expressing 12/15-lipoxygenase

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Y Takahashi
  • ,
  • H Zhu
  • ,
  • WP Xu
  • ,
  • T Murakami
  • ,
  • T Iwasaki
  • ,
  • H Hattori
  • ,
  • T Yoshimoto

338
1
開始ページ
128
終了ページ
135
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2005.07.182
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Oxidation of low density lipoprotein (LDL) is a critical step for atherogenesis, and the role of the 12/15-lipoxygenase (12/15-LOX) as well as LDL receptor-related protein (LRP) expressed in macrophages in this process has been suggested. The oxygenation of cholesteryl linoleate in LDL by mouse macrophage-like J774A.1 cells overexpressing 12/15-LOX was inhibited by an anti-LRP antibody but not by an anti-LDL receptor antibody. When the cells were incubated with LDL double-labeled by [H-3]cholesteryl linoleate and [I-125]apoB, association with the cells of [H-3]cholesteryl linoleate expressed as LDL protein equivalent exceeded that of [I-125]apoB, indicating selective uptake of [H-3]cholesteryl linoleate from LDL to these cells. An anti-LRP antibody inhibited the selective uptake of [H-3]cholesteryl ester by 62% and 81%, with the 12/15-LOX-expressing cells and macrophages, respectively. Furthermore, addition of LDL to the culture medium of the [3H]cholesteryl linoleate-labeled 12/15-LOX-expressing cells increased the release of [H-3]cholesteryl linoleate to the medium in LDL concentration- and time-dependent manners. The transport of [H-3]cholesteryl linoleate from the cells to LDL was also inhibited by an anti-LRP antibody by 75%. These results strongly suggest that LRP contributes to the LDL oxidation by 12/15-LOX in macrophages by selective uptake and efflux of cholesteryl ester in the LDL particle. (c) 2005 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2005.07.182
CiNii Articles
http://ci.nii.ac.jp/naid/80017627134
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/16105647
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000233296700020&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2005.07.182
  • ISSN : 0006-291X
  • CiNii Articles ID : 80017627134
  • PubMed ID : 16105647
  • Web of Science ID : WOS:000233296700020

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