Neuronal protection in stroke by an sLe(x)-glycosylated complement inhibitory protein

Judy Huang, Louis J. Kim, Richard Mealey, Henry C. Marsh, Yuan Zhang, Andrea J. Tenner, E. Sander Connolly, David J. Pinsky

Research output: Contribution to journalArticlepeer-review

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 (sCR1sLe(x)) to inhibit complement activation and endothelial-platelet-leukocyte interactions, sCR1 and sCR1sLe(x) 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.

Original languageEnglish (US)
Pages (from-to)595-599
Number of pages5
JournalScience
Volume285
Issue number5427
DOIs
StatePublished - Jul 23 1999

ASJC Scopus subject areas

  • General

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