Neuronal protection in stroke by an sLex-glycosylated complement inhibitory protein.
Science
; 285(5427): 595-9, 1999 Jul 23.
Article
en En
| MEDLINE
| ID: mdl-10417391
ABSTRACT
Glycoprotein adhesion receptors such as selectins contribute to tissue injury in stroke. Ischemic neurons strongly expressed C1q, which may target them for complement-mediated attack or C1qRp-mediated clearance. A hybrid molecule was used to simultaneously inhibit both complement activation and selectin-mediated adhesion. The extracellular domain of soluble complement receptor-1 (sCR1) was sialyl Lewis x glycosylated (sCR1sLex) to inhibit complement activation and endothelial-platelet-leukocyte interactions. sCR1 and sCR1sLex colocalized to ischemic cerebral microvessels and C1q-expressing neurons, inhibited neutrophil and platelet accumulation, and reduced cerebral infarct volumes. Additional benefit was conferred by sialyl Lewis x glycosylation of the unmodified parent sCR1 molecule.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Oligosacáridos
/
Receptores de Complemento
/
Ataque Isquémico Transitorio
/
Trastornos Cerebrovasculares
/
Fármacos Neuroprotectores
Idioma:
En
Revista:
Science
Año:
1999
Tipo del documento:
Article
País de afiliación:
Estados Unidos