Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/422
Title: The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1<sup>G93A</sup> Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes
Authors: Serrano, Alessia
Donno, Claudia
Giannetti, Stefano
Perić, Mina 
Anđus, Pavle 
D'Ambrosi, Nadia
Michetti, Fabrizio
Issue Date: 20-Jun-2017
Journal: Mediators of Inflammation
Abstract: 
© 2017 Alessia Serrano et al. 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 SOD1G93A mice limits the expression of reactivity-linked/proinflammatory genes. Thus, our results propose the S100B-RAGE axis as an effective contributor to the pathogenesis of the disease, suggesting its blockade as a rational target for a therapeutic intervention in ALS.
URI: https://biore.bio.bg.ac.rs/handle/123456789/422
ISSN: 0962-9351
DOI: 10.1155/2017/1626204
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