Neuronal pathophysiology featuring PrPC and its control over Ca2+ metabolism. Issue 1 (2nd January 2018)

• Record Type: Journal Article
• Authors: Bertoli, Alessandro; Sorgato, M. Catia
• Is Part Of: Prion. Volume 12:Issue 1(2018)
• Page Start: 28
• Page End: 33
• Publication Date: 2018-01-02
• Subjects: Cellular prion protein -- PrPC -- prions -- Ca2+ -- store-operated Ca2+ entry -- glutamate receptors -- excitotoxicity -- knock-out mice -- neurons -- Aβ oligomers; Protein folding -- Periodicals; Prions -- Periodicals; Proteins -- Biotechnology -- Periodicals; 572.633
• DOI: 10.1080/19336896.2017.1412912
• Languages: English
• ISSNs: 1933-6896

Abstract

ABSTRACT: Calcium (Ca 2+ ) is an intracellular second messenger that ubiquitously masters remarkably diverse biological processes, including cell death. Growing evidence substantiates an involvement of the prion protein (PrP C ) in regulating neuronal Ca 2+ homeostasis, which could rationalize most of the wide range of functions ascribed to the protein. We have recently demonstrated that PrP C controls extracellular Ca 2+ fluxes, and mitochondrial Ca 2+ uptake, in neurons stimulated with glutamate (De Mario et al., J Cell Sci 2017; 130:2736-46), suggesting that PrP C protects neurons from threatening Ca 2+ overloads and excitotoxicity. In light of these results and of recent reports in the literature, here we review the connection of PrP C with Ca 2+ metabolism and also provide some speculative hints on the physiologic outcomes of this link. In addition, because PrP C is implicated in neurodegenerative diseases, including prion disorders and Alzheimer's disease, we will also discuss possible ways by which disruption of PrP C -Ca 2+ association could be mechanistically connected with these pathologies.