GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism.
Publication/Presentation Date
2-6-2007
Abstract
The cause of 95% of Parkinson's disease (PD) cases is unknown. It is hypothesized that PD arises from an interaction of free-radical-generating agents with an underlying genetic susceptibility to these compounds. Here we use the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of parkinsonism to examine the role of a dual function protein, GSTpi, in dopaminergic neuron death. GSTpi is the only GST family member expressed in substantia nigra neurons. GSTpi reduction by pharmacological blockade, RNA inhibition, and gene targeting increases sensitivity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, suggesting that differential expression of GSTpi contributes to the sensitivity to xenobiotics in the substantia nigra and may influence the pathogenesis of reactive oxygen species-induced neurological disorders including PD.
Volume
104
Issue
6
First Page
1977
Last Page
1982
ISSN
0027-8424
Published In/Presented At
Smeyne, M., Boyd, J., Raviie Shepherd, K., Jiao, Y., Pond, B. B., Hatler, M., Wolf, R., Henderson, C., & Smeyne, R. J. (2007). GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism. Proceedings of the National Academy of Sciences of the United States of America, 104(6), 1977–1982. https://doi.org/10.1073/pnas.0610978104
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
17267597
Department(s)
Administration and Leadership
Document Type
Article