The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
The HMGB1 Receptor RAGE Mediates Ischemic Brain Damage
Open accessAbstract
In ischemic stroke, the necrotic core is surrounded by a zone of inflammation, in which delayed cell death aggravates the initial insult. Here, we provide evidence that the receptor for advanced glycation end products (RAGE) functions as a sensor of necrotic cell death and contributes to inflammation and ischemic brain damage. The RAGE ligand high mobility group box 1 (HMGB1) was elevated in serum of stroke patients and was released from ischemic brain tissue in a mouse model of cerebral ischemia. A neutralizing anti-HMGB1 antibody and HMGB1 box A, an antagonist of HMGB1 at the receptor RAGE, ameliorated ischemic brain damage. Interestingly, genetic RAGE deficiency and the decoy receptor soluble RAGE reduced the infarct size.In vitro, expression of RAGE in (micro)glial cells mediated the toxic effect of HMGB1. Addition of macrophages to neural cultures further enhanced the toxic effect of HMGB1. To test whether immigrant macrophages in the ischemic brain mediate the RAGE effect, we generated chimeric mice by transplanting RAGE−/−bone marrow to wild-type mice. RAGE deficiency in bone marrow-derived cells significantly reduced the infarct size. Thus, HMGB1–RAGE signaling links necrosis with macrophage activation and may provide a target for anti-inflammatory therapy in stroke.
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Cites
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
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RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
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Self-citationRAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain
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Self-citationUnderstanding RAGE, the receptor for advanced glycation end products
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Self-citationMicroglia in the adult brain arise from Ly-6ChiCCR2+ monocytes only under defined host conditions
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High‐mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity
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Cortical spreading depression causes and coincides with tissue hypoxia
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Cited by
HMGB1 is a therapeutic target for sterile inflammation and infection
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Self-citationNeuroinflammation: friend and foe for ischemic stroke
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Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release
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“, 2007), ischemia/reperfusion of the heart and the brain (Andrassy et al., 2008; Muhammad et al., 2008), and other ailments, may be entirely attributable to the reduced recruitment of inflammatory cells in the injured tissue.”
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Metadata
- Authors
- Muhammad, S., Barakat, W., Stoyanov, S., Murikinati, S., Yang, H., Tracey, K. J., Bendszus, M., Rossetti, G., Nawroth, P. P., Bierhaus, A., & Schwaninger, M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-11-12
- Volume
- 28
- Issue
- 46
- Pages
- 12023-12031
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2147259348
- Cited by
- 412
- References
- 11
- FWCI
- 13.33
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Muhammad, S., Barakat, W., Stoyanov, S., Murikinati, S., Yang, H., Tracey, K. J., Bendszus, M., Rossetti, G., Nawroth, P. P., Bierhaus, A., & Schwaninger, M. (2008). The HMGB1 Receptor RAGE Mediates Ischemic Brain Damage. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.2435-08.2008
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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