2001年9月
Nitric oxide and its decomposed derivatives decrease the binding of extracellular-superoxide dismutase to the endothelial cell surface
FEBS LETTERS
- ,
- ,
- 巻
- 505
- 号
- 2
- 開始ページ
- 296
- 終了ページ
- 300
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/S0014-5793(01)02839-3
- 出版者・発行元
- ELSEVIER SCIENCE BV
Extracellular-superoxide dismutase (EC-SOD) is bound to the vascular endothelial cell surface with an affinity for heparan sulfate proteoglycan. The binding of EC-SOD to the human umbilical vein endothelial cell (HIUVEC) and bovine aortic endothelial cell surface proteoglycans was significantly decreased by the incubation with S-nitroso-N-acetyl-DL-penicillamine (SNAP) and (+/-)-N-[(E)-4-ethyl-2-[(Z)-hydroxyimino]-5-nitro-3-hexene-1-yl]-3-pyridine carboxamide (NOR4), potent nitric oxide (NO) donors. NO derived from lipopolysaccharide-stimulated J774 A-1 cells also decreased the binding of EC-SOD to HIUVEC, and this decrease was blocked by N-G-nitro-L-arginine, a nitric oxide synthase inhibitor. SNAP and NOR4 also decreased the binding of EC-SOD to immobilized heparin. Furthermore, the decomposed derivatives of NO donors and sodium nitrite decreased the binding of EC-SOD. These observations suggest that excess NO produced in the inflammatory conditions decreases the binding of EC-SOD to the vascular endothelial cell surface, which results in a loss of the ability to protect the endothelial cell surface from oxidative stress. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
- リンク情報
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- DOI
- https://doi.org/10.1016/S0014-5793(01)02839-3
- CiNii Articles
- http://ci.nii.ac.jp/naid/80012681961
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/11566193
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000171125800018&DestApp=WOS_CPL
- ID情報
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- DOI : 10.1016/S0014-5793(01)02839-3
- ISSN : 0014-5793
- CiNii Articles ID : 80012681961
- PubMed ID : 11566193
- Web of Science ID : WOS:000171125800018