TY - JOUR
T1 - Modulation of RAGE isoforms expression in the brain and plasma of rats exposed to transient focal cerebral ischemia
AU - Greco, Rosaria
AU - Amantea, Diana
AU - Mangione, Antonina Stefania
AU - Petrelli, Francesco
AU - Gentile, Rocco
AU - Nappi, Giuseppe
AU - Blandini, Fabio
AU - Corasaniti, M. Tiziana
AU - Tassorelli, Cristina
PY - 2012/7
Y1 - 2012/7
N2 - 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.
AB - 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.
KW - Full-length RAGE
KW - MCAo Neuroinflammation
KW - sRAGE Cerebral ischemia/reperfusion
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U2 - 10.1007/s11064-012-0778-1
DO - 10.1007/s11064-012-0778-1
M3 - Article
C2 - 22528836
AN - SCOPUS:84862868438
SN - 0364-3190
VL - 37
SP - 1508
EP - 1516
JO - Neurochemical Research
JF - Neurochemical Research
IS - 7
ER -