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J. Esteve, L. Campello, R. Bru-Martínez, M.-T. Herrero, N. Cuenca, J. Martín-Nieto; Differential Expression of Proteins in the Retina of Parkinsonian Monkeys: A Proteomics Approach. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3991.
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Systemic injection of MPTP to monkeys elicits the appearance of a parkinsonian syndrome including a set of morphological and functional impairments in the retina. The etiology of idiopathic Parkinson’s disease has been associated with intracellular neuronal oxidative damage. Here we have undertaken a proteomics approach in order to identify proteins differentially expressed in the retina of MPTP-treated, parkinsonian monkeys.
Monkeys (Macaca fascicularis) were treated for 2-3 years with MPTP (0.3 mg/kg, i.v.) and then left untreated for 1 additional year. Proteins were solubilized from the neural retinas of control and MPTP-treated animals, labeled with different fluorophores and run pairwise on DIGE gels. Polypeptides showing statistically-significant differences in their expression levels were excised from preparative 2D gels, trypsinized and subjected to MALDI-TOF mass spectrometry analysis. Protein database interrogation was performed by using the MASCOT search engine.
Out of over 700 protein spots resolved on 2D DIGE gels, ca. 30 polypeptides were detected to show a significant underexpression in the parkinsonian monkey retina, whereas one polypeptide was found overexpressed. Their peptide mass fingerprints obtained by MALDI-TOF were used to search the NCBInr database. A number of the identified differentially-expressed polypeptides corresponded to proteins involved in NO toxicity and cellular energy metabolism.
We have identified in the MPTP monkey model of idiopathic Parkinson’s disease a set of retinal proteins showing abnormal expression levels in comparison with healthy subjects, in most cases being downregulated. A number of them could be related to an impairment in energy metabolism and oxidative damage, in keeping with one of the prevalent molecular mechanisms underlying the etiology of parkinsonism.
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