Fas expression promotes proteasomal activity in toxin-induced parkinsonism.

Abstract:

OBJECTIVE:Fas (CD95), commonly categorised as a death receptor due to its well-defined role in apoptosis, can paradoxically also promote neuroprotection. We have previously found that defects in Fas signalling render mice highly susceptible to neural degeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease (PD). Decreased activity of the ubiquitin proteasome system and accumulation of protein aggregates are implicated in PD pathogenesis. Here, we investigate the relationship between Fas and ubiquitin proteasomal activity in neuronal cells. METHODS:We performed proteasome assays in neuroblastoma cells and in midbrain cultures of wild-type and Fas-deficient mice. RESULTS:Neuroblastoma cells upregulated proteasomal activity in response to an activating Fas antibody in vitro. Furthermore, neural tissue from Fas-deficient mice showed decreased proteasomal activity compared with the tissue from wild-type mice when exposed to a PD-inducing toxin in vivo. CONCLUSION:These findings suggest that mechanisms for Fas-mediated neuroprotection may include Fas-induced upregulation of proteasomal activity, and consequently less accumulation of toxic protein aggregates.

journal_name

Acta Neuropsychiatr

journal_title

Acta neuropsychiatrica

authors

Landau AM,Siegrist-Johnstone R,Desbarats J

doi

10.1111/j.1601-5215.2011.00615.x

subject

Has Abstract

pub_date

2012-06-01 00:00:00

pages

166-71

issue

3

eissn

0924-2708

issn

1601-5215

pii

S0924270800026144

journal_volume

24

pub_type

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