Modulation of RAGE isoforms expression in the brain and plasma of rats exposed to transient focal cerebral ischemia

Rosaria Greco, Diana Amantea, Antonina Stefania Mangione, Francesco Petrelli, Rocco Gentile, Giuseppe Nappi, Fabio Blandini, M. Tiziana Corasaniti, Cristina Tassorelli

Research output: Contribution to journalArticlepeer-review


Activation of RAGE (receptor for advanced glycation endproducts) and of its subtypes may play a role in neuronal damage and neuroinflammation associated with brain ischemia, though the underlying mechanisms remain unclear. In this study, we have examined by Western blotting the expression of RAGE isoforms in the cerebral cortex and striatum of Wistar rats subjected to transient (1 or 2 h) middle cerebral artery occlusion (tMCAo). The findings show that the full-length RAGE (*50 kDa) and its isoforms in the 26-43 kDa range are significantly decreased in the ischemic cortex, but not in the striatum, after 1 and 2 h tMCAo when compared to the sham group. By contrast, in the striatum, ischemia-reperfusion injury caused a significant increase of full-length RAGE and its isoforms in the 72-100 kDa range.We also investigated the soluble form of RAGE, which was significantly decreased in the plasma of rats subjected to transient or permanent MCAo. In conclusion, the present data demonstrate that regional brain expression of RAGE is differentially affected by tMCAo in rat. These modifications are accompanied by a decrease in the plasma levels of soluble RAGE, thereby suggesting a potential role for soluble RAGE as a peripheral biomarker of focal ischemia.

Original languageEnglish
Pages (from-to)1508-1516
Number of pages9
JournalNeurochemical Research
Issue number7
Publication statusPublished - Jul 2012


  • Full-length RAGE
  • MCAo Neuroinflammation
  • sRAGE Cerebral ischemia/reperfusion

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Biochemistry


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