論文

査読有り
2004年8月

Oxidized phospholipids in oxidized low-density lipoprotein reduce the activity of tissue factor pathway inhibitor through association with its carboxy-terminal region

ANTIOXIDANTS & REDOX SIGNALING
  • N Ohkura
  • ,
  • S Hiraishi
  • ,
  • H Itabe
  • ,
  • T Hamuro
  • ,
  • YI Kamikubo
  • ,
  • T Takano
  • ,
  • J Matsuda
  • ,
  • S Horie

6
4
開始ページ
705
終了ページ
712
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1089/1523086041361686
出版者・発行元
MARY ANN LIEBERT, INC

Tissue factor pathway inhibitor (TFPI) is a Kunitz-type protease inhibitor that inhibits the initial reactions of blood coagulation. In this study, we explored the nature of active components that reduce the anticoagulant activity of TFPI in oxidized low-density lipoprotein (ox-LDL). The organic solvent-soluble fraction obtained from ox-LDL was fractionated by normal-phase HPLC. The binding profile of each fraction to TFPI showed a single peak eluting near purified oxidized phospholipid. To explore further the components in oxidized phospholipid that inhibit TFPI activity, we used oxidized phospholipids that mimic the biological activity of ox-LDL. The oxidation products of 1- and/or 2-oleoyl phosphatidylcholine or phosphatidylethanolamine were the most potent inhibitors of TFPI activity, whereas those of arachidonyl phosphatidylcholine possessed only a weak inhibitory effect on the TFPI activity. These oxidized phospholipids mainly associated with the C-terminal basic region of the TFPI molecule. The results indicate that oxidation products of delta-9 unsaturated phospholipids are candidate active components of ox-LDL that impair the function of TFPI through specific association with its C-terminal basic region.


リンク情報
DOI
https://doi.org/10.1089/1523086041361686
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000223106400004&DestApp=WOS_CPL
ID情報
  • DOI : 10.1089/1523086041361686
  • ISSN : 1523-0864
  • eISSN : 1557-7716
  • Web of Science ID : WOS:000223106400004

エクスポート
BibTeX RIS