TY  - JOUR
AU  - Serrano, Alessia
AU  - Donno, Claudia
AU  - Giannetti, Stefano
AU  - Perić, Mina
AU  - Andjus, Pavle R.
AU  - D'Ambrosi, Nadia
AU  - Michetti, Fabrizio
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1074
AB  - 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(G93A) 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.
PB  - Hindawi Ltd, London
T2  - Mediators of Inflammation
T1  - The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes
SP  - 1626204
VL  - 2017
DO  - 10.1155/2017/1626204
ER  - 

@article{
author = "Serrano, Alessia and Donno, Claudia and Giannetti, Stefano and Perić, Mina and Andjus, Pavle R. and D'Ambrosi, Nadia and Michetti, Fabrizio",
year = "2017",
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(G93A) 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.",
publisher = "Hindawi Ltd, London",
journal = "Mediators of Inflammation",
title = "The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes",
pages = "1626204",
volume = "2017",
doi = "10.1155/2017/1626204"
}

Serrano, A., Donno, C., Giannetti, S., Perić, M., Andjus, P. R., D'Ambrosi, N.,& Michetti, F.. (2017). The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes. in Mediators of Inflammation
Hindawi Ltd, London., 2017, 1626204.
https://doi.org/10.1155/2017/1626204

Serrano A, Donno C, Giannetti S, Perić M, Andjus PR, D'Ambrosi N, Michetti F. The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes. in Mediators of Inflammation. 2017;2017:1626204.
doi:10.1155/2017/1626204 .

Serrano, Alessia, Donno, Claudia, Giannetti, Stefano, Perić, Mina, Andjus, Pavle R., D'Ambrosi, Nadia, Michetti, Fabrizio, "The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes" in Mediators of Inflammation, 2017 (2017):1626204,
https://doi.org/10.1155/2017/1626204 . .