1. Sodium valproate does not augment Prpsc in murine neuroblastoma cells
- Author
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Pascal Clayette, Thibault Andrieu, Christophe Legendre, Domnique Dormont, and Fabrice Casagrande
- Subjects
Gene isoform ,Time Factors ,Chlorpromazine ,Prions ,animal diseases ,Sodium ,chemistry.chemical_element ,Scrapie ,Biology ,Toxicology ,Murine neuroblastoma ,Mice ,Neuroblastoma ,Cell Line, Tumor ,medicine ,Animals ,Enzyme Inhibitors ,Regulation of gene expression ,Valproic Acid ,General Neuroscience ,medicine.disease ,Virology ,Molecular biology ,nervous system diseases ,Gene Expression Regulation ,chemistry ,Dopamine Antagonists ,lipids (amino acids, peptides, and proteins) ,medicine.drug - Abstract
Sodium valproate (VPA) has been reported to increase the accumulation of the pathologic isoform of prion protein (PrPsc) in scrapie-infected murine neuroblastoma cells. In this study, the effect of VPA on PrPsc accumulation was investigated in murine N2a neuroblastoma cells chronically infected with scrapie strain 22L (N2a-22L). No accumulation of PrPsc was detected after short-term (3 days) or long-term (21 days) treatment of N2a-22L cells with 4.8, 12, 18 or 24 microM VPA. Higher VPA concentrations (240 and 600 microM) also failed to augment PrPsc expression. In conclusion, in our experimental conditions, no deleterious effect was induced by VPA on prions replication.
- Published
- 2007
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