Linked Life Data

18619530

Source:http://linkedlifedata.com/resource/pubmed/id/18619530

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-10-17
pubmed:abstractText
The cellular mechanisms that may underlie the death of dopaminergic neurons in Parkinson's disease are ubiquitin-proteasomal system (UPS) impairment, mitochondrial dysfunction, and oxidative stress. The goal of this work was to elucidate the correlation between mitochondrial dysfunction and UPS impairment, focusing on the role of oxidative stress. Our data revealed that mitochondria-DNA-depleted cells (rho0) are compromised at the mitochondrial and UPS levels and also show an alteration of the oxidative status. In parental cells (rho+), MPP(+) induced a clear inhibition of complex I activity, as well as an increase in ubiquitinylated protein levels, which was not observed in cells treated with lactacystin. Moreover, MPP(+) induced a decreased in the 20S chymotrypsin-like and peptidyl-glutamyl peptide hydrolytic-like proteolytic activities after 24 h of exposure. ROS production was increased in rho+ cells treated with MPP(+) or lactacystin, at early treatment periods. MPP(+) induced an increase in carbonyl group formation in rho+ cells. The results suggest that a mitochondrial alteration leads to an imbalance in the cellular oxidative status, inducing a proteasomal deregulation, which may exacerbate protein aggregation, and consequently degenerative events.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0891-5849
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
820-5
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Mitochondria and ubiquitin-proteasomal system interplay: relevance to Parkinson's disease.
pubmed:affiliation
Center for Neurosciences and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't