PXD000838 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | Mitochondrial proteomics investigation of a cellular model of impaired dopamine homeostasis, an early step in Parkinson's disease pathogenesis |
Description | Impaired dopamine homeostasis is an early event in the pathogenesis of Parkinson's disease. Generation of intracellular reactive oxygen species consequent to dopamine oxidation leads to mitochondrial dysfunction and eventually cell death. Alterations in the mitochondrial proteome due to dopamine exposure were investigated in the SH-SY5Y human neuroblastoma cell line. The combination of two orthogonal proteomic approaches, two-dimensional electrophoresis and shotgun proteomics, was used to highlight the specific pathways perturbed by the increase of intracellular dopamine, in comparison with those perturbed by a specific mitochondrial toxin (4-methyphenylpyridinium, MPP+), a neurotoxin causing Parkinsonism-like symptoms in animal models. Proteins altered by MPP+ did not completely overlap with those affected by dopamine treatment. In particular, the MPP+ target complex I component NADH dehydrogenase [ubiquinone] iron-sulfur protein 3 was not affected by dopamine together with 26 other proteins. The comparison of proteomics approaches highlighted the fragmentation of some mitochondrial proteins, suggesting an alteration of the mitochondrial protease activity. Pathway and disease association analysis of the proteins affected by dopamine revealed the overrepresentation of the Parkinson's disease and the parkin-ubiquitin proteasomal system pathways and of gene ontologies associated to generation of precursor metabolites and energy, response to topologically incorrect proteins and programmed cell death. These alterations may be globally interpreted in part as the result of a direct effect of dopamine on mitochondria (e.g. alteration of the mitochondrial protease activity) and in part as the effect on mitochondria of a general activation of cellular processes (e.g. regulation of programmed cell death). |
HostingRepository | PRIDE |
AnnounceDate | 2014-07-24 |
AnnouncementXML | Submission_2014-07-24_03:56:42.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | Luisa Pieroni |
SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: 9606; |
ModificationList | monohydroxylated residue; iodoacetamide derivatized residue |
Instrument | Synapt MS |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2014-03-17 08:34:36 | ID requested | |
1 | 2014-04-15 07:15:47 | announced | |
⏵ 2 | 2014-07-24 03:56:42 | announced | Updated project metadata. |
Publication List
Alberio T, Bondi H, Colombo F, Alloggio I, Pieroni L, Urbani A, Fasano M, Mitochondrial proteomics investigation of a cellular model of impaired dopamine homeostasis, an early step in Parkinson's disease pathogenesis. Mol Biosyst, 10(6):1332-44(2014) [pubmed] |
Keyword List
ProteomeXchange project tag: Biology/Disease-Driven Human Proteome Project (B/D-HPP), Human Proteome Project |
curator keyword: Biomedical |
submitter keyword: Dopamine |
Human Proteome Project |
Mitochondria |
MPP+ |
Parkinson's disease |
Respiratory chain |
Shotgun proteomics |
MSe |
Contact List
Andrea Urbani |
contact affiliation | Department of Experimental Medicine and Surgery, University of Rome "Tor Vergata", Rome, and Santa Lucia IRCCS Foundation, Rome, Italy |
contact email | andrea.urbani@uniroma2.it |
lab head | |
Luisa Pieroni |
contact affiliation | Proteomics and Metabonomics Laboratory, CERC- S.Lucia Foundation Rome , AND Italy and Dep. of Surgery and Experimental Medicine, Faculty of Surgery and Medicine, University of Rome "Tor Vergata" Rome, Italy |
contact email | luisa.pieroni@uniroma2.it |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
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PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD000838
- Label: PRIDE project
- Name: Mitochondrial proteomics investigation of a cellular model of impaired dopamine homeostasis, an early step in Parkinson's disease pathogenesis