ArticleScientific reports2017
HMGB1/Advanced Glycation End Products (RAGE) does not aggravate inflammation but promote endogenous neural stem cells differentiation in spinal cord injury.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Injection of BMSCs into the tail vertebrae vein of mice promotes spinal cord repair by inhibiting the HMGB1/RAGE signaling pathway after acute contusive spinal cord injury.In vitro cellular & developmental biology. Animal · 2025Article
- NT-3 Combined with TGF-β Signaling Pathway Enhance the Repair of Spinal Cord Injury by Inhibiting Glial Scar Formation and Promoting Axonal Regeneration.Molecular biotechnology · 2024Article
- High-Mobility Group Box 1 in Spinal Cord Injury and Its Potential Role in Brain Functional Remodeling After Spinal Cord Injury.Cellular and molecular neurobiology · 2023Review
- Role of RAGE in the Pathogenesis of Neurological Disorders.Neuroscience bulletin · 2022Review
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
- HMGB1 Promotes the Release of Sonic Hedgehog From Astrocytes.Frontiers in immunology · 2021Article
- Transplantation of neural stem cells preconditioned with high‑mobility group box 1 facilitates functional recovery after spinal cord injury in rats.Molecular medicine reports · 2020Article
- Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury.Journal of neuroinflammation · 2020Article
- Spinal cord injury can be relieved by the polysaccharides of Tricholoma matsutake by promoting axon regeneration and reducing neuroinflammation.Neuroreport · 2020Article
- Microglia Receptors in Animal Models of Traumatic Brain Injury.Molecular neurobiology · 2019Review
- The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.Neurochemistry international · 2019Review
- HMGB1-modified mesenchymal stem cells attenuate radiation-induced vascular injury possibly via their high motility and facilitation of endothelial differentiation.Stem cell research & therapy · 2019Article
- Receptor for Advanced Glycation End-Products (RAGE) Blockade Do Damage to Neuronal Survival via Disrupting Wnt/β-Catenin Signaling in Spinal Cord Injury.Neurochemical research · 2018Article
- High-mobility group box 1 facilitates migration of neural stem cells via receptor for advanced glycation end products signaling pathway.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor for advanced glycation end products (RAGE) signaling is involved in a series of cell functions after spinal cord injury (SCI). Our study aimed to elucidate the effects of RAGE signaling on the neuronal recovery after SCI. In vivo, rats were subjected to SCI with or without anti-RAGE antibodies micro-injected into the lesion epicenter. We detected Nestin/RAGE, SOX-2/RAGE and Nestin/MAP-2 after SCI by Western blot or immunofluorescence (IF). We found that neural stem cells (NSCs) co-expressed with RAGE were significantly activated after SCI, while stem cell markers Nestin and SOX-2 were reduced by RAGE blockade. We found that RAGE inhibition reduced nestin-positive NSCs expressing MAP-2, a mature neuron marker. RAGE blockade does not improve neurobehavior Basso, Beattie and Bresnahan (BBB) scores; however, it damaged survival of ventral neurons via Nissl staining. Through in vitro study, we found that recombinant HMGB1 administration does not lead to increased cytokines of TNF-α and IL-1β, while anti-RAGE treatment reduced cytokines of TNF-α and IL-1β induced by LPS via ELISA. Meanwhile, HMGB1 increased MAP-2 expression, which was blocked after anti-RAGE treatment. Hence, HMGB1/RAGE does not exacerbate neuronal inflammation but plays a role in promoting NSCs differentiating into mature neurons in the pathological process of SCI.
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