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 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.

[1]  B. Kleinschmidt-DeMasters,et al.  Dual use of E-cadherin and D2-40 immunostaining in unusual meningioma subtypes. , 2015, American journal of clinical pathology.

[2]  K. Gupta,et al.  Mechanism of Nanotization-Mediated Improvement in the Efficacy of Caffeine Against 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism. , 2015, Journal of biomedical nanotechnology.

[3]  J. Forrester,et al.  Evidence for a role of adaptive immune response in the disease pathogenesis of the MPTP mouse model of Parkinson's disease , 2015, Glia.

[4]  Jia-wei Zhou,et al.  Neuroinflammation in Parkinson’s disease and its potential as therapeutic target , 2015, Translational Neurodegeneration.

[5]  M. Kaplitt,et al.  The tumor suppressor PTEN regulates motor responses to striatal dopamine in normal and Parkinsonian animals , 2015, Neurobiology of Disease.

[6]  P. De Baetselier,et al.  E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo , 2015, Scientific Reports.

[7]  N. Sikka,et al.  Expression and Significance of Cadherins and Its Subtypes in Development and Progression of Oral Cancers: A Review. , 2015, Journal of clinical and diagnostic research : JCDR.

[8]  E. Fornasiero,et al.  Cadherins as regulators of neuronal polarity , 2015, Cell adhesion & migration.

[9]  Qing Zhou,et al.  Enhanced expression of suppresser of cytokine signaling 3 inhibits the IL-6-induced epithelial-to-mesenchymal transition and cholangiocarcinoma cell metastasis , 2015, Medical Oncology.

[10]  C. Niu,et al.  Comparing neuroprotective effects of CDNF-expressing bone marrow derived mesenchymal stem cells via differing routes of administration utilizing an in vivo model of Parkinson’s disease , 2015, Neurological Sciences.

[11]  O. Barreiro,et al.  Caveolin-1 deficiency induces a MEK-ERK1/2-Snail-1-dependent epithelial–mesenchymal transition and fibrosis during peritoneal dialysis , 2014, EMBO molecular medicine.

[12]  E. Hirsch,et al.  Heat shock protein 60: an endogenous inducer of dopaminergic cell death in Parkinson disease , 2014, Journal of Neuroinflammation.

[13]  E. Hirsch,et al.  Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease , 2013, Scientific Reports.

[14]  T. Zuo,et al.  Involvement of N-cadherin in the protective effect of glial cell line-derived neurotrophic factor on dopaminergic neuron damage. , 2013, International journal of molecular medicine.

[15]  F. Curcio,et al.  Observing the mouse thyroid sphingomyelin under space conditions: a case study from the MDS mission in comparison with hypergravity conditions. , 2012, Astrobiology.

[16]  F. Curcio,et al.  The thyroid lobes: the different twins. , 2012, Archives of biochemistry and biophysics.

[17]  Juliette van Steenwinckel,et al.  Neurochemokines: a menage a trois providing new insights on the functions of chemokines in the central nervous system , 2011, Journal of neurochemistry.

[18]  S. Shimohama,et al.  N-cadherin Regulates p38 MAPK Signaling via Association with JNK-associated Leucine Zipper Protein , 2010, The Journal of Biological Chemistry.

[19]  F. Cicchetti,et al.  Differences between subacute and chronic MPTP mice models: investigation of dopaminergic neuronal degeneration and α‐synuclein inclusions , 2009, Journal of neurochemistry.

[20]  E. Hirsch,et al.  Neuroinflammation in Parkinson's disease: a target for neuroprotection? , 2009, The Lancet Neurology.

[21]  M. V. Magni,et al.  Lipid microdomains in cell nucleus. , 2008, Molecular biology of the cell.

[22]  D. Surmeier,et al.  Modeling PD pathogenesis in mice: advantages of a chronic MPTP protocol. , 2008, Parkinsonism & related disorders.

[23]  J. Potashkin,et al.  MPTP administration in mice changes the ratio of splice isoforms of fosB and rgs9 , 2007, Brain Research.

[24]  E. Hirsch,et al.  The Role of Glial Reaction and Inflammation in Parkinson's Disease , 2003, Annals of the New York Academy of Sciences.

[25]  S. Mandel,et al.  Early and late molecular events in neurodegeneration and neuroprotection in Parkinson’s disease MPTP model as assessed by cDNA microarray; the role of iron , 2002, Neurotoxicity Research.

[26]  S. Totterdell,et al.  Mouse model of Parkinsonism: a comparison between subacute MPTP and chronic MPTP/probenecid treatment , 2001, Neuroscience.

[27]  T. Nagatsu,et al.  Interleukin (IL)-1β, IL-2, IL-4, IL-6 and transforming growth factor-α levels are elevated in ventricular cerebrospinal fluid in juvenile parkinsonism and Parkinson's disease , 1996, Neuroscience Letters.

[28]  A. Lees,et al.  Ageing and Parkinson's disease: substantia nigra regional selectivity. , 1991, Brain : a journal of neurology.