e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease

Today a large number of studies are focused on clarifying the complexity and diversity of the pathogenetic mechanisms inducing Parkinson disease. We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin that induces Parkinson disease, to evaluate the change of midbrain structure and...

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Main Authors: Samuela Cataldi, Michela Codini, Stéphane Hunot, François-Pierre Légeron, Ivana Ferri, Paola Siccu, Angelo Sidoni, Francesco Saverio Ambesi-Impiombato, Tommaso Beccari, Francesco Curcio, Elisabetta Albi
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2016/3937057
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author Samuela Cataldi
Michela Codini
Stéphane Hunot
François-Pierre Légeron
Ivana Ferri
Paola Siccu
Angelo Sidoni
Francesco Saverio Ambesi-Impiombato
Tommaso Beccari
Francesco Curcio
Elisabetta Albi
author_facet Samuela Cataldi
Michela Codini
Stéphane Hunot
François-Pierre Légeron
Ivana Ferri
Paola Siccu
Angelo Sidoni
Francesco Saverio Ambesi-Impiombato
Tommaso Beccari
Francesco Curcio
Elisabetta Albi
author_sort Samuela Cataldi
collection DOAJ
description Today a large number of studies are focused on clarifying the complexity and diversity of the pathogenetic mechanisms inducing Parkinson disease. We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin that induces Parkinson disease, to evaluate the change of midbrain structure and the behavior of the anti-inflammatory factor e-cadherin, interleukin-6, tyrosine hydroxylase, phosphatase and tensin homolog, and caveolin-1. The results showed a strong expression of e-cadherin, variation of length and thickness of the heavy neurofilaments, increase of interleukin-6, and reduction of tyrosine hydroxylase known to be expression of dopamine cell loss, reduction of phosphatase and tensin homolog described to impair responses to dopamine, and reduction of caveolin-1 known to be expression of epithelial-mesenchymal transition and fibrosis. The possibility that the overexpression of the e-cadherin might be implicated in the anti-inflammatory reaction to MPTP treatment by influencing the behavior of the other analyzed molecules is discussed.
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spelling doaj-art-67b29e679f68432384a3602c860f3ce72025-02-03T01:21:36ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/39370573937057e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson DiseaseSamuela Cataldi0Michela Codini1Stéphane Hunot2François-Pierre Légeron3Ivana Ferri4Paola Siccu5Angelo Sidoni6Francesco Saverio Ambesi-Impiombato7Tommaso Beccari8Francesco Curcio9Elisabetta Albi10Department of Pharmaceutical Science, University of Perugia, 06100 Perugia, ItalyDepartment of Pharmaceutical Science, University of Perugia, 06100 Perugia, ItalyInserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle ÉPINIÈRE, ICM, 75013 Paris, FranceInserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle ÉPINIÈRE, ICM, 75013 Paris, FranceInstitute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, ItalyInstitute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, ItalyInstitute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, ItalyDepartment of Clinical and Biological Sciences, University of Udine, 33100 Udine, ItalyDepartment of Pharmaceutical Science, University of Perugia, 06100 Perugia, ItalyDepartment of Clinical and Biological Sciences, University of Udine, 33100 Udine, ItalyDepartment of Pharmaceutical Science, University of Perugia, 06100 Perugia, ItalyToday a large number of studies are focused on clarifying the complexity and diversity of the pathogenetic mechanisms inducing Parkinson disease. We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin that induces Parkinson disease, to evaluate the change of midbrain structure and the behavior of the anti-inflammatory factor e-cadherin, interleukin-6, tyrosine hydroxylase, phosphatase and tensin homolog, and caveolin-1. The results showed a strong expression of e-cadherin, variation of length and thickness of the heavy neurofilaments, increase of interleukin-6, and reduction of tyrosine hydroxylase known to be expression of dopamine cell loss, reduction of phosphatase and tensin homolog described to impair responses to dopamine, and reduction of caveolin-1 known to be expression of epithelial-mesenchymal transition and fibrosis. The possibility that the overexpression of the e-cadherin might be implicated in the anti-inflammatory reaction to MPTP treatment by influencing the behavior of the other analyzed molecules is discussed.http://dx.doi.org/10.1155/2016/3937057
spellingShingle Samuela Cataldi
Michela Codini
Stéphane Hunot
François-Pierre Légeron
Ivana Ferri
Paola Siccu
Angelo Sidoni
Francesco Saverio Ambesi-Impiombato
Tommaso Beccari
Francesco Curcio
Elisabetta Albi
e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
Mediators of Inflammation
title e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
title_full e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
title_fullStr e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
title_full_unstemmed e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
title_short e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
title_sort e cadherin in 1 methyl 4 phenyl 1 2 3 6 tetrahydropyridine induced parkinson disease
url http://dx.doi.org/10.1155/2016/3937057
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