S100B is an astrocytic cytokine that has been shown to be involved in several neurodegenerative diseases. We used an astrocytoma cell line (U373 MG) silenced for S100B, and stimulated it with amyloid beta-peptide (Aβ) as a known paradigm factor for astrocyte activation, and showed that the ability of the cell (including the gene machinery) to express S100B is a prerequisite for inducing reactive astrocytic features, such as ROS generation, NOS activation and cytotoxicity. Our results showed that control astrocytoma cell line exhibited overexpression of S100B after Aβ treatment, and subsequently cytotoxicity, increased ROS generation and NOS activation. In contrast, cells silenced with S100B were essentially protected, consistently reducing cell death, significantly decreasing oxygen radical generation and nitric oxide synthase activity. The conclusive aim of the present study was to show a causative linkage between the cell expression of S100B and induction of astrocyte activation processes, such as cytotoxicity, ROS and NOS activation.

Clementi, M. E., Sampaolese, B., Di Sante, G., Ria, F., Di Liddo, R., Romano Spica, V., Michetti, F., S100B Expression Plays a Crucial Role in Cytotoxicity, Reactive Oxygen Species Generation and Nitric Oxide Synthase Activation Induced by Amyloid β-Protein in an Astrocytoma Cell Line, <<INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES>>, 2023; 24 (6): N/A-N/A. [doi:10.3390/ijms24065213] [https://hdl.handle.net/10807/303944]

S100B Expression Plays a Crucial Role in Cytotoxicity, Reactive Oxygen Species Generation and Nitric Oxide Synthase Activation Induced by Amyloid β-Protein in an Astrocytoma Cell Line

Di Sante, Gabriele;Ria, Francesco;Michetti, Fabrizio
2023

Abstract

S100B is an astrocytic cytokine that has been shown to be involved in several neurodegenerative diseases. We used an astrocytoma cell line (U373 MG) silenced for S100B, and stimulated it with amyloid beta-peptide (Aβ) as a known paradigm factor for astrocyte activation, and showed that the ability of the cell (including the gene machinery) to express S100B is a prerequisite for inducing reactive astrocytic features, such as ROS generation, NOS activation and cytotoxicity. Our results showed that control astrocytoma cell line exhibited overexpression of S100B after Aβ treatment, and subsequently cytotoxicity, increased ROS generation and NOS activation. In contrast, cells silenced with S100B were essentially protected, consistently reducing cell death, significantly decreasing oxygen radical generation and nitric oxide synthase activity. The conclusive aim of the present study was to show a causative linkage between the cell expression of S100B and induction of astrocyte activation processes, such as cytotoxicity, ROS and NOS activation.
2023
AREA05 - SCIENZE BIOLOGICHE
Pubblicazione su rivista con Impact Factor
Inglese
Articolo in rivista
Inglese
S100B
amyloid beta peptide
astrocytes
Settore MEDS-02/B - Patologia clinica
Multidisciplinary Digital Publishing Institute (MDPI)
24
6
2023
N/A
N/A
5213
Goal 3: Good health and well-being
info:eu-repo/semantics/article
Clementi, M. E., Sampaolese, B., Di Sante, G., Ria, F., Di Liddo, R., Romano Spica, V., Michetti, F., S100B Expression Plays a Crucial Role in Cytotoxicity, Reactive Oxygen Species Generation and Nitric Oxide Synthase Activation Induced by Amyloid β-Protein in an Astrocytoma Cell Line, <<INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES>>, 2023; 24 (6): N/A-N/A. [doi:10.3390/ijms24065213] [https://hdl.handle.net/10807/303944]
open
262
Clementi, Maria Elisabetta; Sampaolese, Beatrice; Di Sante, Gabriele; Ria, Francesco; Di Liddo, Rosa; Romano Spica, Vincenzo; Michetti, Fabrizio...espandi
7
art_per_29
03. Contributo in rivista::Articolo in rivista, Nota a sentenza
File in questo prodotto:
File Dimensione Formato  
ijms-24-05213-v2.pdf

accesso aperto

Tipologia file ?: Versione Editoriale (PDF)
Licenza: Creative commons
Dimensione 1.3 MB
Formato Adobe PDF
1.3 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10807/303944
Citazioni
  • ???jsp.display-item.citation.pmc??? 9
  • Scopus 10
  • ???jsp.display-item.citation.isi??? 10
social impact