Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-4-16
pubmed:abstractText
Parkinson's disease (PD) is associated with perturbed mitochondrial function. Studies of cytoplasmic hybrid (cybrid) cell lines containing mitochondria from PD subjects suggest complex I dysfunction in particular is a relatively upstream biochemical defect. To evaluate potential downstream consequences of PD mitochondrial dysfunction, we used a cybrid approach to model PD mitochondrial dysfunction; our cybrid cell lines were generated via transfer of PD or control subject platelet mitochondria to mtDNA-depleted NT2 cells. To confirm our PD cybrid mitochondria did indeed differ from control cybrid mitochondria we measured complex I V(max) activities. Consistent with other PD cybrid reports, relative to control cybrid cell lines the PD cybrid cell line mean complex I V(max) activity was reduced. In this validated model, we used an oxygen electrode to characterize PD cybrid mitochondrial respiration. Although whole cell basal oxygen consumption was comparable between the PD and control cybrid groups, the proton leak was increased and maximum respiratory capacity was decreased in the PD cybrids. PD cybrids also had reduced SIRT1 phosphorylation, reduced peroxisome proliferator-activated receptor-gamma coactivator-1alpha levels, and increased NF-kB activation. We conclude mitochondrial respiration and pathways influenced by aerobic metabolism are altered in NT2 cybrid cell lines generated through transfer of PD subject platelet mitochondria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1471-4159
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
674-82
pubmed:dateRevised
2010-7-6
pubmed:meshHeading
pubmed-meshheading:20132468-Aerobiosis, pubmed-meshheading:20132468-Aged, pubmed-meshheading:20132468-Anaerobiosis, pubmed-meshheading:20132468-Blotting, Western, pubmed-meshheading:20132468-Cell Line, pubmed-meshheading:20132468-Cell Respiration, pubmed-meshheading:20132468-Citrate (si)-Synthase, pubmed-meshheading:20132468-Electron Transport Complex I, pubmed-meshheading:20132468-Enzyme Activation, pubmed-meshheading:20132468-Humans, pubmed-meshheading:20132468-Hybrid Cells, pubmed-meshheading:20132468-Kinetics, pubmed-meshheading:20132468-Middle Aged, pubmed-meshheading:20132468-Mitochondria, pubmed-meshheading:20132468-NF-kappa B, pubmed-meshheading:20132468-Oxygen Consumption, pubmed-meshheading:20132468-Parkinson Disease, pubmed-meshheading:20132468-Protons, pubmed-meshheading:20132468-Sirtuin 1
pubmed:year
2010
pubmed:articleTitle
Mitochondrial respiration and respiration-associated proteins in cell lines created through Parkinson's subject mitochondrial transfer.
pubmed:affiliation
Centro de Neurociências e Biologia Celular, Universidade de Coimbra, Coimbra, Portugal.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't