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

Abstract

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.

• 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
• Journal: Mediators of inflammation (Mediators Inflamm) Vol. 2016 Pg. 3937057 ( 2016) ISSN: 1466-1861 [Electronic] United States
• PMID: 27194825 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cadherins
• Interleukin-6
• 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
• Tyrosine 3-Monooxygenase

Topics

• 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)
• Animals
• Cadherins (metabolism)
• Interleukin-6 (metabolism)
• Male
• Mice, Inbred C57BL
• Parkinson Disease (etiology, metabolism)
• Tyrosine 3-Monooxygenase (metabolism)