Neuronal RAGE expression modulates severity of injury following transient focal cerebral ischemia

Benjamin G. Hassid, M. Nathan Nair, Andrew F. Ducruet, Marc L. Otten, Ricardo J. Komotar, David J. Pinsky, Ann Marie Schmidt, Shi Fang Yan, E. Sander Connolly

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Inflammation has a significant role in the neurological injury that follows stroke. The receptor for advanced-glycation end products (RAGE) is a multiligand member of the immunoglobulin superfamily that has been implicated in multiple neuronal and inflammatory stress processes. To directly test the role of neuronal RAGE in stroke, we employed two cohorts of transgenic mice, one over-expressing full-length functional human RAGE in neurons, and the other a human RAGE transgene in which deletion of the cytoplasmic domain of the receptor in neurons suppresses signal transduction stimulated by ligands (referred to as dominant negative or DN-RAGE). We found a statistically significant increase in stroke volume in the RAGE over-expressing cohort compared to normal controls, and a trend towards decreased stroke volume in the DN RAGE cohort. These results indicate that RAGE signaling directly contributes to pathology in cerebral ischemia.

Original languageEnglish (US)
Pages (from-to)302-306
Number of pages5
JournalJournal of Clinical Neuroscience
Volume16
Issue number2
DOIs
StatePublished - Feb 2009
Externally publishedYes

Keywords

  • Inflammation
  • Ischemia
  • Murine
  • RAGE
  • Reperfusion
  • Stroke

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology
  • Physiology (medical)

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