ArticleJournal of neuroscience research2008
Expression of the receptor for advanced glycation end products in oligodendrocytes in response to oxidative stress.
Article in Journal of neuroscience research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- The usefulness of immunotherapy in pediatric neurodegenerative disorders: A systematic review of literature data.Human vaccines & immunotherapeutics · 2015Pooled it
- Molecular mechanisms of exercise-induced neuroprotection against Parkinson's disease.Sports medicine and health science · 2026Review
- Are Oligodendrocytes the Culprits or Victims in Alzheimer's Disease.Physiological research · 2025Review
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Dietary galactose exacerbates autoimmune neuroinflammationFrontiers in immunology · 2024Article
- In Vitro Effects of Methylprednisolone over Oligodendroglial Cells: Foresight to Future Cell Therapies.Cells · 2023Article
- Modulating Morphological and Redox/Glycative Alterations in the PCOS Uterus: Effects of Carnitines in PCOS Mice.Biomedicines · 2023Article
- Review
- Intranasal Administration of Undifferentiated Oligodendrocyte Lineage Cells as a Potential Approach to Deliver Oligodendrocyte Precursor Cells into Brain.International journal of molecular sciences · 2021Article
- Advanced glycation end products and their receptors in serum of patients with type 2 diabetes.Scientific reports · 2021Article
- Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury.Journal of neuroinflammation · 2020Article
- RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration.Molecular neurobiology · 2018Review
- RAGE Expression and ROS Generation in Neurons: Differentiation versus Damage.Oxidative medicine and cellular longevity · 2016Review
- Radical roles for RAGE in the pathogenesis of oxidative stress in cardiovascular diseases and beyond.International journal of molecular sciences · 2013Review
- HMGB1 protein does not mediate the inflammatory response in spontaneous spinal cord regeneration: a hint for CNS regeneration.The Journal of biological chemistry · 2013Article
- Amyloid-β production: major link between oxidative stress and BACE1.Neurotoxicity research · 2012Review
- The Receptor for Advanced Glycation End-products (RAGE) protects pancreatic tumor cells against oxidative injury.Antioxidants & redox signaling · 2011Article
- Protein modification by dicarbonyl molecular species in neurodegenerative diseases.Journal of amino acids · 2011Article
- Glial cell lines: an overview.Neurochemical research · 2010Review
- Diagnostic potential of plasma carboxymethyllysine and carboxyethyllysine in multiple sclerosis.Journal of neuroinflammation · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Demyelination is a common result of oxidative stress in the nervous system, and we report here that the response of oligodendrocytes to oxidative stress involves the receptor for advanced glycation end products (RAGE). RAGE has not previously been reported in neonatal rat oligodendrocytes (NRO), but, by using primers specific for rat RAGE, we were able to show expression of messenger RNA (mRNA) for RAGE in NRO, and a 55-kDa protein was detected by Western blotting with antibodies to RAGE. Neonatal rat oligodendrocytes stained strongly for RAGE, suggesting membrane localization of RAGE. Addition of low concentrations of hydrogen peroxide (100 microM) initiated 55-kDa RAGE shedding from the cell membrane and the appearance of "soluble" 45-kDa RAGE in the culture medium, followed by restoration of RAGE expression to normal levels. Increasing hydrogen peroxide concentration (>200 microM) resulted in no restoration of RAGE, and the cells underwent apoptosis and necrosis. We further confirmed the observation in a human oligodendroglioma-derived (HOG) cell line. Both the antioxidant N-acetyl-L-cysteine and the broad-spectrum metalloproteases inhibitor TAPI0 were able partially to inhibit shedding of RAGE, suggesting involvement of metalloproteases in cleavage to produce soluble RAGE. The level of 55-kDa RAGE in autopsy brain of patients undergoing neurodegeneration with accompanying inflammation [multiple sclerosis and neuronal ceroid-lipofuscinosis (Batten's disease)] was much lower than that in age-matched controls, suggesting that shedding of RAGE might occur as reactive oxygen species accumulate in brain cells and be part of the process of neurodegeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.