Journal
NEUROSCIENCE LETTERS
Volume 459, Issue 1, Pages 11-15Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2009.04.060
Keywords
Mitochondria; Nucleolin; Oxidative stress; Parkinson disease; Proteasome; Substantia nigra pars compacta
Categories
Funding
- National Institutes of Health [AG025327, ES012703, T32007032]
- Michael J. Fox Foundation
- American Parkinson's Disease Association
- C.-M. Shaw Endowment
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Although much has been learned in the last few decades concerning the molecular mechanisms and pathways associated with the development of familial as well as sporadic Parkinson disease (PD), the precise mechanisms and specific proteins responsible for mediating these effects remain to be elucidated. Thus, the identification and biological evaluation of novel proteins involved in these pathways is critical to providing a more comprehensive understanding of PD pathogenesis. Previously, in a cellular model of PD, we identified nucleolin as a protein interacting with alpha-synuclein and DJ-1, two critical proteins involved in PD pathogenesis. In our current study, we found the expression levels of nucleolin were dramatically reduced in the substantia nigra pars compacta of human PD subjects, compared with controls. Furthermore. manipulation of nucleolin in an in vitro model of PD resulted in significant alterations in the generation of oxidative stress as well as proteasomal inhibition following rotenone exposure. Interestingly, nucleolin expression did not influence mitochondrial complex I activity, suggesting a selective specificity for oxidative stress and proteasomal pathways. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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