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Titolo:
Ulex europaeus agglutinin II (UEA-II) is a novel, potent inhibitor of complement activation
Autore:
Lekowski, R; Collard, CD; Reenstra, WR; Stahl, GL;
Indirizzi:
Harvard Univ, Brigham & Womens Hosp, Sch Med,Dept Anesthesiol Perioperat &Pain Med, Ctr Expt Therapeut & Reperfus Injury, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 & Reperfus Injury, Boston, MA 02115 USA Beth Israel Deaconess Hosp, Dept Emergency Med, Boston, MA 02118 USA Beth Israel Deaconess Hosp Boston MA USA 02118 Med, Boston, MA 02118 USA
Titolo Testata:
PROTEIN SCIENCE
fascicolo: 2, volume: 10, anno: 2001,
pagine: 277 - 284
SICI:
0961-8368(200102)10:2<277:UEAI(I>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEMBRANE ATTACK COMPLEX; VEIN ENDOTHELIAL-CELLS; MANNAN-BINDING LECTIN; MYOCARDIAL-ISCHEMIA; SERINE-PROTEASE; REPERFUSION; EXPRESSION; PATHWAY; HYPOXIA; INJURY;
Keywords:
hypoxia; reoxygenation; mannose-binding lectin; neutrophils; chemotaxis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Stahl, GL Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Anesthesia,Ctr Expt Therapeut & Reperfus Inj, 75 Francis St, Boston, MA 02115 USA Harvard Univ 75 Francis St Boston MA USA 02115 ton, MA 02115 USA
Citazione:
R. Lekowski et al., "Ulex europaeus agglutinin II (UEA-II) is a novel, potent inhibitor of complement activation", PROTEIN SCI, 10(2), 2001, pp. 277-284

Abstract

Complement is an important mediator of vascular injury following oxidativestress. We recently demonstrated that complement activation following endothelial oxidative stress is mediated by mannose-binding lectin (MBL) and activation of the lectin complement pathway. Here, we investigated whether nine plant lectins which have a binding profile similar to that of MBL competitively inhibit MBL deposition and subsequent complement activation following human umbilical vein endothelial cell (HUVEC) oxidative stress. HUVEC oxidative stress (1% O-2, 24 hr) significantly increased Ulex europaeus agglutinin II (UEA-II) binding by 72 +/- 9% compared to normoxic cells. UEA-II inhibited MBL binding to HUVEC in a concentration-dependent manner followingoxidative stress. Further, MBL inhibited UEA-II binding to HUVEC in a concentration-dependent manner following oxidative stress, suggesting a common ligand. UEA-II (less than or equal to 100 mu mol/L) did not attenuate the hemolytic activity, nor did it inhibit C3a des Arg formation from alternative or classical complement pathway-specific hemolytic assays. C3 deposition (measured by ELISA) following HUVEC oxidative stress was inhibited by UEA-II in a concentration-dependent manner (IC50 = 10 pmol/L). UEA-II inhibited C3 and MBL co-localization (confocal microscopy) in a concentration-dependent manner on HUVEC following oxidative stress (IC50 approximate to 1 pmol/L). Finally, UEA-II significantly inhibited complement-dependent neutrophil chemotaxis, but failed to inhibit fMLP-mediated chemotaxis, following endothelial oxidative stress. These data demonstrate that UEA-II is a novel, potent inhibitor of human MBL deposition and complement activation following human endothelial oxidative stress.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/12/17 alle ore 23:37:45