e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
Identifieur interne : 000143 ( Pmc/Curation ); précédent : 000142; suivant : 000144e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease
Auteurs : Samuela Cataldi [Italie] ; Michela Codini [Italie] ; Stéphane Hunot [France] ; François-Pierre Légeron [France] ; Ivana Ferri [Italie] ; Paola Siccu [Italie] ; Angelo Sidoni [Italie] ; Francesco Saverio Ambesi-Impiombato [Italie] ; Tommaso Beccari [Italie] ; Francesco Curcio [Italie] ; Elisabetta Albi [Italie]Source :
- Mediators of Inflammation [ 0962-9351 ] ; 2016.
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.
Url:
DOI: 10.1155/2016/3937057
PubMed: 27194825
PubMed Central: 4852763
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uniqKey="Legeron F" first="François-Pierre" last="Légeron">François-Pierre Légeron</name><affiliation wicri:level="1"><nlm:aff id="I2">Inserm 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, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>Inserm 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</wicri:regionArea></affiliation></author><author><name sortKey="Ferri, Ivana" sort="Ferri, Ivana" uniqKey="Ferri I" first="Ivana" last="Ferri">Ivana Ferri</name><affiliation wicri:level="1"><nlm:aff id="I3">Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia</wicri:regionArea></affiliation></author><author><name sortKey="Siccu, Paola" sort="Siccu, Paola" uniqKey="Siccu P" first="Paola" last="Siccu">Paola Siccu</name><affiliation wicri:level="1"><nlm:aff id="I3">Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia</wicri:regionArea></affiliation></author><author><name sortKey="Sidoni, Angelo" sort="Sidoni, Angelo" uniqKey="Sidoni A" first="Angelo" last="Sidoni">Angelo Sidoni</name><affiliation wicri:level="1"><nlm:aff id="I3">Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia</wicri:regionArea></affiliation></author><author><name sortKey="Ambesi Impiombato, Francesco Saverio" sort="Ambesi Impiombato, Francesco Saverio" uniqKey="Ambesi Impiombato F" first="Francesco Saverio" last="Ambesi-Impiombato">Francesco Saverio Ambesi-Impiombato</name><affiliation wicri:level="1"><nlm:aff id="I4">Department of Clinical and Biological Sciences, University of Udine, 33100 Udine, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Clinical and Biological Sciences, University of Udine, 33100 Udine</wicri:regionArea></affiliation></author><author><name sortKey="Beccari, Tommaso" sort="Beccari, Tommaso" uniqKey="Beccari T" first="Tommaso" last="Beccari">Tommaso Beccari</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Pharmaceutical Science, University of Perugia, 06100 Perugia, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Pharmaceutical Science, University of Perugia, 06100 Perugia</wicri:regionArea></affiliation></author><author><name sortKey="Curcio, Francesco" sort="Curcio, Francesco" uniqKey="Curcio F" first="Francesco" last="Curcio">Francesco Curcio</name><affiliation wicri:level="1"><nlm:aff id="I4">Department of Clinical and Biological Sciences, University of Udine, 33100 Udine, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Clinical and Biological Sciences, University of Udine, 33100 Udine</wicri:regionArea></affiliation></author><author><name sortKey="Albi, Elisabetta" sort="Albi, Elisabetta" uniqKey="Albi E" first="Elisabetta" last="Albi">Elisabetta Albi</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Pharmaceutical Science, University of Perugia, 06100 Perugia, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Pharmaceutical Science, University of Perugia, 06100 Perugia</wicri:regionArea></affiliation></author></analytic><series><title level="j">Mediators of Inflammation</title><idno type="ISSN">0962-9351</idno><idno type="eISSN">1466-1861</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Meredith, G E" uniqKey="Meredith G">G. E. Meredith</name></author><author><name sortKey="Totterdell, S" uniqKey="Totterdell S">S. Totterdell</name></author><author><name sortKey="Potashkin, J A" uniqKey="Potashkin J">J. A. Potashkin</name></author><author><name sortKey="Surmeier, D J" uniqKey="Surmeier D">D. J. Surmeier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fearnley, J M" uniqKey="Fearnley J">J. M. Fearnley</name></author><author><name sortKey="Lees, A J" uniqKey="Lees A">A. J. Lees</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Potashkin, J A" uniqKey="Potashkin J">J. A. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Mediators Inflamm</journal-id><journal-id journal-id-type="iso-abbrev">Mediators Inflamm</journal-id><journal-id journal-id-type="publisher-id">MI</journal-id><journal-title-group><journal-title>Mediators of Inflammation</journal-title></journal-title-group><issn pub-type="ppub">0962-9351</issn><issn pub-type="epub">1466-1861</issn><publisher><publisher-name>Hindawi Publishing Corporation</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">27194825</article-id><article-id pub-id-type="pmc">4852763</article-id><article-id pub-id-type="doi">10.1155/2016/3937057</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Cataldi</surname><given-names>Samuela</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Codini</surname><given-names>Michela</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hunot</surname><given-names>Stéphane</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Légeron</surname><given-names>François-Pierre</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ferri</surname><given-names>Ivana</given-names></name><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Siccu</surname><given-names>Paola</given-names></name><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sidoni</surname><given-names>Angelo</given-names></name><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ambesi-Impiombato</surname><given-names>Francesco Saverio</given-names></name><xref ref-type="aff" rid="I4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Beccari</surname><given-names>Tommaso</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Curcio</surname><given-names>Francesco</given-names></name><xref ref-type="aff" rid="I4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Albi</surname><given-names>Elisabetta</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Department of Pharmaceutical Science, University of Perugia, 06100 Perugia, Italy</aff><aff id="I2"><sup>2</sup>Inserm 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, France</aff><aff id="I3"><sup>3</sup>Institute of Pathologic Anatomy and Histology, University of Perugia, 06100 Perugia, Italy</aff><aff id="I4"><sup>4</sup>Department of Clinical and Biological Sciences, University of Udine, 33100 Udine, Italy</aff><author-notes><corresp id="cor1">*Elisabetta Albi: <email>elisabetta.albi@gmail.com</email></corresp><fn fn-type="other"><p>Academic Editor: Francisco López-Muñoz</p></fn></author-notes><pub-date pub-type="ppub"><year>2016</year></pub-date><pub-date pub-type="epub"><day>17</day><month>4</month><year>2016</year></pub-date><volume>2016</volume><elocation-id>3937057</elocation-id><history><date date-type="received"><day>12</day><month>1</month><year>2016</year></date><date date-type="accepted"><day>29</day><month>3</month><year>2016</year></date></history><permissions><copyright-statement>Copyright © 2016 Samuela Cataldi et al.</copyright-statement><copyright-year>2016</copyright-year><license license-type="open-access"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>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.</p></abstract></article-meta></front><floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label><caption><p>Midbrain of untreated (control) or MPTP-treated (experimental) mice. The samples were treated as reported in <xref ref-type="sec" rid="sec2">Section 2</xref>. (a) Phase contrast images of substantia nigra, 10x magnification; (b) neurofilament 200 kDa (NF200) immunohistochemical staining, 4x magnification, (c) 20x magnification, and (d) 100x magnification. The arrows indicate the effect of MPTP treatment in the reduction of area with neurofilaments (a) and of length and thickness of neurofilaments (b, c, d).</p></caption><graphic xlink:href="MI2016-3937057.001"></graphic></fig><fig id="fig2" orientation="portrait" position="float"><label>Figure 2</label><caption><p>(a) Immunoblotting analysis of e-cadherin, tyrosine hydroxylase (TH), interleukin-6 (IL-6), PTEN, and caveolin-1. The position of the proteins was evaluated in relation to that of molecular size standards. (b) The area density was quantified by densitometry scanning and analysis with Scion Image; the data represent the mean ± SD of three separated experiments. <sup><italic>∗</italic></sup><italic>P</italic> < 0.001 versus control sample.</p></caption><graphic xlink:href="MI2016-3937057.002"></graphic></fig><fig id="fig3" orientation="portrait" position="float"><label>Figure 3</label><caption><p>(a) Fluorescence immunostaining of e-cadherin and tyrosine hydroxylase (TH) by using specific antibodies in the substantia nigra area of control and experimental midbrain. 40x magnification. (b) The immunofluorescence area density was quantified by densitometry scanning and analysis with Scion Image; the data represent the mean ± SD of three separated experiments. <sup><italic>∗</italic></sup><italic>P</italic> < 0.001 versus control sample. The arrows indicate the distribution of e-cadherin and TH fluorescence; e-cadherin is randomly distributed in control sample and has specific localization around the soma in experimental sample. TH florescence is evident around the neurons and along the neurofilaments in control sample whereas it is distributed uniformly in the tissue surrounding the cells.</p></caption><graphic xlink:href="MI2016-3937057.003"></graphic></fig></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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