ArticleMediators of inflammation2017
The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1
Article in Mediators of inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Relationship of S100 Proteins with Neuroinflammation.Biomolecules · 2025Review
- Effect on Different Glial Cell Types of S100B Modulation in Multiple Sclerosis Experimental Models.International journal of molecular sciences · 2025Article
- Article
- Novel insights into RAGE signaling pathways during the progression of amyotrophic lateral sclerosis in RAGE-deficient SOD1 G93A mice.PloS one · 2024Article
- The Key Role of Astrocytes in Amyotrophic Lateral Sclerosis and Their Commitment to Glutamate Excitotoxicity.International journal of molecular sciences · 2023Review
- Article
- The S100B Protein: A Multifaceted Pathogenic Factor More Than a Biomarker.International journal of molecular sciences · 2023Review
- Striatal spatial heterogeneity, clustering, and white matter association of GFAPFrontiers in cellular neuroscience · 2023Article
- Receptors for Advanced Glycation End Products (RAGE): Promising Targets Aiming at the Treatment of Neurodegenerative Conditions.Current neuropharmacology · 2023Review
- Role of RAGE in the Pathogenesis of Neurological Disorders.Neuroscience bulletin · 2022Review
- Perinatal exposure to synergistic multiple stressors leads to cellular and behavioral deficits mimicking Schizophrenia-like pathology.Biology open · 2022Article
- The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice.International journal of molecular sciences · 2022Article
- Role and Therapeutic Potential of RAGE Signaling in Neurodegeneration.Current drug targets · 2022Article
- Cognitive dysfunction associated with COVID-19: Prognostic role of circulating biomarkers and microRNAs.Frontiers in aging neuroscience · 2022Review
- Microglia RAGE exacerbates the progression of neurodegeneration within the SOD1Journal of neuroinflammation · 2021Article
- Recovery of Depleted miR-146a in ALS Cortical Astrocytes Reverts Cell Aberrancies and Prevents Paracrine Pathogenicity on Microglia and Motor Neurons.Frontiers in cell and developmental biology · 2021Article
- [SBi4211 alleviates gp120-induced central nervous system injuryNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Absence of Receptor for Advanced Glycation End Product (RAGE) Reduces Inflammation and Extends Survival in the hSOD1Molecular neurobiology · 2020Article
- UCHL1 from serum and CSF is a candidate biomarker for amyotrophic lateral sclerosis.Annals of clinical and translational neurology · 2020Article
- The S100B Protein and Partners in Adipocyte Response to Cold Stress and Adaptive Thermogenesis: Facts, Hypotheses, and Perspectives.Biomolecules · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is one of the major players in amyotrophic lateral sclerosis (ALS) pathogenesis, and astrocytes are significantly involved in this process. The astrocytic protein S100B can be released in pathological states activating the receptor for advanced glycation end products (RAGE). Different indications point to an aberrant expression of S100B and RAGE in ALS. In this work, we observed that S100B and RAGE are progressively and selectively upregulated in astrocytes of diseased rats with a tissue-specific timing pattern, correlated to the level of neurodegeneration. The expression of the full-length and soluble RAGE isoforms could also be linked to the degree of tissue damage. The mere presence of mutant SOD1 is able to increase the intracellular levels and release S100B from astrocytes, suggesting the possibility that an increased astrocytic S100B expression might be an early occurring event in the disease. Finally, our findings indicate that the protein may exert a proinflammatory role in ALS, since its inhibition in astrocytes derived from SOD1
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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.