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Titolo:
A keratin peptide inhibits mannose-binding lectin
Autore:
Montalto, MC; Collard, CD; Buras, JA; Reenstra, WR; McClaine, R; Gies, DR; Rother, RP; Stahl, GL;
Indirizzi:
Harvard Univ, Sch Med,Dept Anesthesiol Perioperat & Pain Med, Brigham & Womens Hosp, 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 02115 USA Beth Israel Deaconess Hosp Boston MA USA 02115 Med, Boston, MA 02115 USA Alexion Pharmaceut Inc, New Haven, CT 06511 USA Alexion Pharmaceut Inc New Haven CT USA 06511 nc, New Haven, CT 06511 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 6, volume: 166, anno: 2001,
pagine: 4148 - 4153
SICI:
0022-1767(20010315)166:6<4148:AKPIML>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-ADHESION MOLECULE-1; SURFACE-PLASMON RESONANCE; BETA-D-GLUCOSAMINE; ENDOTHELIAL-CELLS; COMPLEMENT ACTIVATION; GLOMERULAR DEPOSITION; RHEUMATIC CARDITIS; ANTIBODY-RESPONSE; SERINE-PROTEASE; PATHWAY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Stahl, GL Harvard Univ, Sch Med,Dept Anesthesiol Perioperat & Pain Med, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, 75 Francis St, Boston, MA 02115 USA Harvard Univ 75 Francis St Boston MA USA 02115 ton, MA 02115 USA
Citazione:
M.C. Montalto et al., "A keratin peptide inhibits mannose-binding lectin", J IMMUNOL, 166(6), 2001, pp. 4148-4153

Abstract

Complement plays a significant role in mediating endothelial injury following oxidative stress. We have previously demonstrated that the lectin complement pathway (LCP), which is initiated by deposition of the mannose-binding lectin (MBL), is largely responsible for activating complement on endothelial cells following periods of oxidative stress. Identifying functional inhibitors that block MBL binding will be useful in characterizing the role of the LCP in disease models. The human cytokeratin peptide SFGSGFGGGY has been identified as a molecular mimic of N-acetyl-D-glucosamine (GlcNAc), a known ligand of MBL. Thus, we hypothesized that this peptide would specifically bind to MBL and functionally inhibit the LCP on endothelial cells following oxidative stress. Using a BIAcore 3000 optical biosensor, competition experiments were performed to demonstrate that the peptide SFGSGFGGGY inhibits binding of purified recombinant human MBL to GlcNAc in a concentration dependent manner. Solution affinity data generated by BIAcore indicate thispeptide binds to MBL with an affinity (K-D) of 5 x 10(-5) mol/L. Pretreatment of human serum (30%) with the GlcNAc-mimicking peptide (10-50 mug/ml) significantly attenuated MBL and C3 deposition on human endothelial cells subjected to oxidative stress in a dose-dependent manner, as demonstrated by cell surface ELISA and confocal microscopy, Additionally, this decapeptide sequence attenuated complement-dependent VCAM-1 expression following oxidative stress. These data indicate that a short peptide sequence that mimics GlcNAc can specifically bind to MBL and functionally inhibit the proinflammatory action of the LCP on oxidatively stressed endothelial cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 17:53:57