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Cellular prion protein offers neuroprotection in astrocytes submitted to amyloid ß oligomer toxicity.
Marques, Caroline M S; Gomes, Rafael N; Pedron, Tatiana; Batista, Bruno L; Cerchiaro, Giselle.
Afiliação
  • Marques CMS; Center for Natural Sciences and Humanities, Federal University of ABC - UFABC, Avenida dos Estados, 5001, Santo André, SP, 09210-580, Brazil.
  • Gomes RN; Metal Biochemistry and Oxidative Stress Lab, Center for Natural Sciences and Humanities, Federal University of ABC - UFABC, Avenida dos Estados, 5001, Bloco B, Santo André, SP, 09210-580, Brazil.
  • Pedron T; Center for Natural Sciences and Humanities, Federal University of ABC - UFABC, Avenida dos Estados, 5001, Santo André, SP, 09210-580, Brazil.
  • Batista BL; Metal Biochemistry and Oxidative Stress Lab, Center for Natural Sciences and Humanities, Federal University of ABC - UFABC, Avenida dos Estados, 5001, Bloco B, Santo André, SP, 09210-580, Brazil.
  • Cerchiaro G; Center for Natural Sciences and Humanities, Federal University of ABC - UFABC, Avenida dos Estados, 5001, Santo André, SP, 09210-580, Brazil.
Mol Cell Biochem ; 478(8): 1847-1865, 2023 Aug.
Article em En | MEDLINE | ID: mdl-36576715
The cellular prion protein (PrPC), in its native conformation, performs numerous cellular and cognitive functions in brain tissue. However, despite the cellular prion research in recent years, there are still questions about its participation in oxidative and neurodegenerative processes. This study aims to elucidate the involvement of PrPC in the neuroprotection cascade in the presence of oxidative stressors. For that, astrocytes from wild-type mice and knockout to PrPC were subjected to the induction of oxidative stress with hydrogen peroxide (H2O2) and with the toxic oligomer of the amyloid ß protein (AßO). We observed that the presence of PrPC showed resistance in the cell viability of astrocytes. It was also possible to monitor changes in basic levels of metals and associate them with an induced damage condition, indicating the precise role of PrPC in metal homeostasis, where the absence of PrPC leads to metallic unbalance, culminating in cellular vulnerability to oxidative stress. Increased caspase 3, p-Tau, p53, and Bcl2 may establish a relationship between a PrPC and an induced damage condition. Complementarily, it has been shown that PrPC prevents the internalization of AßO and promotes its degradation under oxidative stress induction, thus preventing protein aggregation in astrocytes. It was also observed that the presence of PrPC can be related to translocating SOD1 to cell nuclei under oxidative stress, probably controlling DNA damage. The results of this study suggest that PrPC acts against oxidative stress activating the cellular response and defense by displaying neuroprotection to neurons and ensuring the functionality of astrocytes.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Príons / Proteínas PrPC Limite: Animals Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Brasil País de publicação: Holanda
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Príons / Proteínas PrPC Limite: Animals Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Brasil País de publicação: Holanda