RAGE mediates vascular injury and inflammation after global cerebral ischemia
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.
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RAGE is not known to be related to oxytocin or oxytocin signalling.
“RAGE, a member of the immunoglobulin superfamily of pattern recognition receptors, is not known to be related to oxytocin or oxytocin signalling22–33.”
From Vascular RAGE transports oxytocin into the brain to elicit its maternal bonding behaviour in mice (2019) · cites this paper as [23]
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- Authors
- Kamide, T., Kitao, Y., Takeichi, T., Okada, A., Mohri, H., Schmidt, A. M., Kawano, T., Munesue, S., Yamamoto, Y., Yamamoto, H., Hamada, J.-I., & Hori, O.
- Affiliations
- Kanazawa University (JP)
- Kanazawa Medical University (JP)
- NYU Langone Health (US)
- Kumamoto University (JP)
- Corresponding author
- Hori, Osamu
- ORCID
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 60
- Issue
- 3
- Pages
- 220-228
- ISSN
- 0197-0186 (ISSN-L)
- OpenAlex
- W2007963813
- Cited by
- 60
- References
- 28
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 4 · 2022: 4 · 2021: 8 · 2020: 5 · 2019: 7 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 6 · 2014: 8 · 2013: 8 · 2012: 2
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurochemistry International (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (23659430)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- receptor for advanced glycation end products, RAGE, global cerebral ischemia, bilateral common carotid artery occlusion, delayed neuronal death, hippocampal CA1, vascular injury, nitrotyrosine, endothelial nitric oxide synthase, inducible nitric oxide synthase, TNF-α, neuroprotection
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Brain Ischemia, Image Processing, Computer-Assisted, Immunohistochemistry, Inflammation, Male, Mice, Inbred C57BL, Mice, Transgenic, Neuroglia, Receptors, Immunologic, Tumor Necrosis Factor-alpha, Tyrosine, Cell Death, Mice, Knockout, Oxidative Stress, Carotid Artery Injuries, Stroke, Mice, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III, Vascular System Injuries, Real-Time Polymerase Chain Reaction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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