The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1^G93A Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes.

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 astr

SUBMITTER: Serrano A 

PROVIDER: S-EPMC5496121 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature