| First Author | Kamide T | Year | 2012 |
| Journal | Neurochem Int | Volume | 60 |
| Issue | 3 | Pages | 220-8 |
| PubMed ID | 22202666 | Mgi Jnum | J:323154 |
| Mgi Id | MGI:6843067 | Doi | 10.1016/j.neuint.2011.12.008 |
| Citation | Kamide T, et al. (2012) RAGE mediates vascular injury and inflammation after global cerebral ischemia. Neurochem Int 60(3):220-8 |
| abstractText | The receptor for advanced glycation end products (RAGE) is a multi-ligand receptor involved in a diverse range of pathological conditions. To analyze the roles of RAGE and its decoy receptor, endogenous secretory RAGE (esRAGE), in the global cerebral ischemia, three different mouse cohorts, wild-type, RAGE(-)/(-), and esRAGE transgenic (Tg) mice were subjected to bilateral common carotid artery occlusion (BCCAO). RT-PCR and immunohistochemical analysis revealed that expression of RAGE was induced in the vascular cells at 12 h, and then in the neurons and glia from 3 to 7 days in the hippocampus after BCCAO. The numbers of surviving neurons in the hippocampal CA1 region were significantly higher in RAGE(-)/(-) and esRAGE Tg mice than those in wild-type mice in the periods between 24 h and 7 days after BCCAO. Lower levels of 3-nitrotyrosine (3-NT) and higher levels of endothelial nitric oxide synthase (eNOS), together with enlarged vascular areas were observed in RAGE(-)/(-) and esRAGE Tg mice at 12 h after BCCAO. In the later periods, expressions of glia-derived inflammatory mediators TNFalpha and inducible nitric oxide synthase (iNOS) were reduced in RAGE(-)/(-) and esRAGE Tg mice. These results suggest that RAGE may contribute to delayed neuronal death after global cerebral ischemia by enhancing vascular injury and deleterious glia-mediated inflammation. |
