ParkinsonFranceV1, Pmc, Curation, bibRecord, 000432

Protective role of olesoxime against wild-type α-synuclein-induced toxicity in human neuronally differentiated SHSY-5Y cells

Identifieur interne : 000432 ( Pmc/Curation ); précédent : 000431; suivant : 000433

Protective role of olesoxime against wild-type α-synuclein-induced toxicity in human neuronally differentiated SHSY-5Y cells

Auteurs : C. Gouarné [France] ; J. Tracz [France] ; M Giraudon Paoli [France] ; V. Deluca [France] ; M. Seimandi [France] ; G. Tardif [France] ; M. Xilouri [Grèce] ; L. Stefanis [Grèce] ; T. Bordet [France] ; R M Pruss [France]

Source :

British Journal of Pharmacology [ 0007-1188 ] ; 2014.

RBID : PMC:4280980

Abstract

BACKGROUND AND PURPOSE

Parkinson's disease (PD) is usually diagnosed clinically from classical motor symptoms, while definitive diagnosis is made postmortem, based on the presence of Lewy bodies and nigral neuron cell loss. α-Synuclein (ASYN), the main protein component of Lewy bodies, clearly plays a role in the neurodegeneration that characterizes PD. Additionally, mutation in the SNCA gene or copy number variations are associated with some forms of familial PD. Here, the objective of the study was to evaluate whether olesoxime, a promising neuroprotective drug can prevent ASYN-mediated neurotoxicity.

EXPERIMENTAL APPROACH

We used here a novel, mechanistically approachable and attractive cellular model based on the inducible overexpression of human wild-type ASYN in neuronally differentiated human neuroblastoma (SHSY-5Y) cells. This model demonstrates gradual cellular degeneration, coinciding temporally with the appearance of soluble and membrane-bound ASYN oligomers and cell death combining both apoptotic and non-apoptotic pathways.

KEY RESULTS

Olesoxime fully protected differentiated SHSY-5Y cells from cell death, neurite retraction and cytoplasmic shrinkage induced by moderate ASYN overexpression. This protection was associated with a reduction in cytochrome c release from mitochondria and caspase-9 activation suggesting that olesoxime prevented ASYN toxicity by preserving mitochondrial integrity and function. In addition, olesoxime displayed neurotrophic effects on neuronally differentiated SHSY-5Y cells, independent of ASYN expression, by promoting their differentiation.

CONCLUSIONS AND IMPLICATIONS

Because ASYN is a common underlying factor in many cases of PD, olesoxime could be a promising therapy to slow neurodegeneration in PD.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280980

DOI: 10.1111/bph.12939
PubMed: 25220617
PubMed Central: 4280980

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Le document en format XML

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<front><div type="abstract" xml:lang="en"><sec><title>BACKGROUND AND PURPOSE</title>
<p>Parkinson's disease (PD) is usually diagnosed clinically from classical motor symptoms, while definitive diagnosis is made postmortem, based on the presence of Lewy bodies and nigral neuron cell loss. α-Synuclein (ASYN), the main protein component of Lewy bodies, clearly plays a role in the neurodegeneration that characterizes PD. Additionally, mutation in the <italic>SNCA</italic>
 gene or copy number variations are associated with some forms of familial PD. Here, the objective of the study was to evaluate whether olesoxime, a promising neuroprotective drug can prevent ASYN-mediated neurotoxicity.</p>
</sec>
<sec><title>EXPERIMENTAL APPROACH</title>
<p>We used here a novel, mechanistically approachable and attractive cellular model based on the inducible overexpression of human wild-type ASYN in neuronally differentiated human neuroblastoma (SHSY-5Y) cells. This model demonstrates gradual cellular degeneration, coinciding temporally with the appearance of soluble and membrane-bound ASYN oligomers and cell death combining both apoptotic and non-apoptotic pathways.</p>
</sec>
<sec><title>KEY RESULTS</title>
<p>Olesoxime fully protected differentiated SHSY-5Y cells from cell death, neurite retraction and cytoplasmic shrinkage induced by moderate ASYN overexpression. This protection was associated with a reduction in cytochrome c release from mitochondria and caspase-9 activation suggesting that olesoxime prevented ASYN toxicity by preserving mitochondrial integrity and function. In addition, olesoxime displayed neurotrophic effects on neuronally differentiated SHSY-5Y cells, independent of ASYN expression, by promoting their differentiation.</p>
</sec>
<sec><title>CONCLUSIONS AND IMPLICATIONS</title>
<p>Because ASYN is a common underlying factor in many cases of PD, olesoxime could be a promising therapy to slow neurodegeneration in PD.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <front><journal-meta><journal-id journal-id-type="nlm-ta">Br J Pharmacol</journal-id>
<journal-id journal-id-type="iso-abbrev">Br. J. Pharmacol</journal-id>
<journal-id journal-id-type="publisher-id">bph</journal-id>
<journal-title-group><journal-title>British Journal of Pharmacology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0007-1188</issn>
<issn pub-type="epub">1476-5381</issn>
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<article-id pub-id-type="doi">10.1111/bph.12939</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Papers</subject>
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<title-group><article-title>Protective role of olesoxime against wild-type α-synuclein-induced toxicity in human neuronally differentiated SHSY-5Y cells</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Gouarné</surname>
<given-names>C</given-names>
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<xref ref-type="aff" rid="au1">1</xref>
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</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Paoli</surname>
<given-names>M Giraudon</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Deluca</surname>
<given-names>V</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Seimandi</surname>
<given-names>M</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tardif</surname>
<given-names>G</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xilouri</surname>
<given-names>M</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Stefanis</surname>
<given-names>L</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
<xref ref-type="aff" rid="au3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bordet</surname>
<given-names>T</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="author-notes" rid="fn1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Pruss</surname>
<given-names>R M</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<aff id="au1"><label>1</label>
<institution>Trophos, Parc Scientifique de Luminy, Luminy Biotech Entreprises</institution>
<addr-line>Marseille, France</addr-line>
</aff>
<aff id="au2"><label>2</label>
<institution>Division of Basic Neurosciences, Biomedical Research Foundation of the Academy of Athens</institution>
<addr-line>Athens, Greece</addr-line>
</aff>
<aff id="au3"><label>3</label>
<institution>Second Department of Neurology, University of Athens Medical School</institution>
<addr-line>Athens, Greece</addr-line>
</aff>
</contrib-group>
<author-notes><corresp id="cor1">Caroline Gouarné, Trophos, Parc Scientifique de Luminy, Luminy Biotech Enterprises, Case 931, 13288 Marseille Cedex 9, France. E-mail: <email>cgouarne@trophos.com</email>
</corresp>
<fn id="fn1" fn-type="present-address"><label>*</label>
<p>Present address: Biotherapies Institute for Rare Diseases, 1 Rue de l'Internationale, Evry 91002, France.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>1</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>01</day>
<month>12</month>
<year>2014</year>
</pub-date>
<volume>172</volume>
<issue>1</issue>
<fpage>235</fpage>
<lpage>245</lpage>
<history><date date-type="received"><day>02</day>
<month>4</month>
<year>2014</year>
</date>
<date date-type="rev-recd"><day>04</day>
<month>9</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>08</day>
<month>9</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>© 2014 The British Pharmacological Society</copyright-statement>
<copyright-year>2014</copyright-year>
</permissions>
<abstract><sec><title>BACKGROUND AND PURPOSE</title>
<p>Parkinson's disease (PD) is usually diagnosed clinically from classical motor symptoms, while definitive diagnosis is made postmortem, based on the presence of Lewy bodies and nigral neuron cell loss. α-Synuclein (ASYN), the main protein component of Lewy bodies, clearly plays a role in the neurodegeneration that characterizes PD. Additionally, mutation in the <italic>SNCA</italic>
 gene or copy number variations are associated with some forms of familial PD. Here, the objective of the study was to evaluate whether olesoxime, a promising neuroprotective drug can prevent ASYN-mediated neurotoxicity.</p>
</sec>
<sec><title>EXPERIMENTAL APPROACH</title>
<p>We used here a novel, mechanistically approachable and attractive cellular model based on the inducible overexpression of human wild-type ASYN in neuronally differentiated human neuroblastoma (SHSY-5Y) cells. This model demonstrates gradual cellular degeneration, coinciding temporally with the appearance of soluble and membrane-bound ASYN oligomers and cell death combining both apoptotic and non-apoptotic pathways.</p>
</sec>
<sec><title>KEY RESULTS</title>
<p>Olesoxime fully protected differentiated SHSY-5Y cells from cell death, neurite retraction and cytoplasmic shrinkage induced by moderate ASYN overexpression. This protection was associated with a reduction in cytochrome c release from mitochondria and caspase-9 activation suggesting that olesoxime prevented ASYN toxicity by preserving mitochondrial integrity and function. In addition, olesoxime displayed neurotrophic effects on neuronally differentiated SHSY-5Y cells, independent of ASYN expression, by promoting their differentiation.</p>
</sec>
<sec><title>CONCLUSIONS AND IMPLICATIONS</title>
<p>Because ASYN is a common underlying factor in many cases of PD, olesoxime could be a promising therapy to slow neurodegeneration in PD.</p>
</sec>
</abstract>
</article-meta>
</front>
</pmc>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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Protective role of olesoxime against wild-type α-synuclein-induced toxicity in human neuronally differentiated SHSY-5Y cells

Protective role of olesoxime against wild-type α-synuclein-induced toxicity in human neuronally differentiated SHSY-5Y cells

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