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RAGE mediates vascular injury and inflammation after global cerebral ischemia.
- Source :
-
Neurochemistry international [Neurochem Int] 2012 Feb; Vol. 60 (3), pp. 220-8. Date of Electronic Publication: 2011 Dec 19. - Publication Year :
- 2012
-
Abstract
- 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 TNFα 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.<br /> (Copyright © 2011 Elsevier Ltd. All rights reserved.)
- Subjects :
- Animals
Carotid Artery Injuries pathology
Cell Death physiology
Image Processing, Computer-Assisted
Immunohistochemistry
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Neuroglia physiology
Nitric Oxide Synthase Type II biosynthesis
Nitric Oxide Synthase Type III biosynthesis
Oxidative Stress physiology
Real-Time Polymerase Chain Reaction
Receptor for Advanced Glycation End Products
Tumor Necrosis Factor-alpha biosynthesis
Tyrosine analogs & derivatives
Tyrosine pharmacology
Brain Ischemia pathology
Inflammation pathology
Receptors, Immunologic physiology
Stroke pathology
Vascular System Injuries pathology
Subjects
Details
- Language :
- English
- ISSN :
- 1872-9754
- Volume :
- 60
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Neurochemistry international
- Publication Type :
- Academic Journal
- Accession number :
- 22202666
- Full Text :
- https://doi.org/10.1016/j.neuint.2011.12.008