ChloroquineV1, Main, Exploration, bibRecord, 000D45

Nanoparticles restore lysosomal acidification defects: Implication for Parkinson and other lysosomal-related diseases.

Identifieur interne : 000D45 ( Main/Exploration ); précédent : 000D44; suivant : 000D46

Nanoparticles restore lysosomal acidification defects: Implication for Parkinson and other lysosomal-related diseases.

Auteurs : Mathieu Bourdenx [France] ; Jonathan Daniel [France] ; Emilie Genin [France] ; Federico N. Soria [France] ; Mireille Blanchard-Desce [France] ; Erwan Bezard [France] ; Benjamin Dehay [France]

Source :

Autophagy [ 1554-8627 ] ; 2016-01-13.

RBID : Hal:hal-01287766

English descriptors

mix :
- ATP13A2, GBA, Parkinson disease, XMEA, lysosome, nanoparticles, neurodegeneration.

Abstract

Lysosomal impairment causes lysosomal storage disorders (LSD) and is involved in pathogenesis of neurodegenerative diseases, notably Parkinson disease (PD). Strategies enhancing or restoring lysosomal-mediated degradation thus appear as tantalising disease-modifying therapeutics. Here we demonstrate that poly(DL-lactide-co-glycolide) (PLGA) acidic nanoparticles (aNP) restore impaired lysosomal function in a series of toxin and genetic cellular models of PD, i.e. ATP13A2-mutant or depleted cells or glucocerebrosidase (GBA)-mutant cells, as well as in a genetic model of lysosomal-related myopathy. We show that PLGA-aNP are transported to the lysosome within 24 h, lower lysosomal pH and rescue chloroquine (CQ)-induced toxicity. Re-acidification of defective lysosomes following PLGA-aNP treatment restores lysosomal function in different pathological contexts. Finally, our results show that PLGA-aNP may be detected after intracerebral injection in neurons and attenuate PD-related neurodegeneration in vivo by mechanisms involving a rescue of compromised lysosomes.

Url:

Affiliations:

Le document en format XML

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<author><name sortKey="Soria, Federico N" sort="Soria, Federico N" uniqKey="Soria F" first="Federico N" last="Soria">Federico N. Soria</name>
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<author><name sortKey="Blanchard Desce, Mireille" sort="Blanchard Desce, Mireille" uniqKey="Blanchard Desce M" first="Mireille" last="Blanchard-Desce">Mireille Blanchard-Desce</name>
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<region type="region" nuts="2">Nouvelle-Aquitaine</region>
<region type="old region" nuts="2">Aquitaine</region>
</placeName>
<orgName type="university">Université de Bordeaux</orgName>
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</author>
<author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
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          <desc>            <address>              <country key="FR"></country>
            </address>
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<country>France</country>
<placeName><settlement type="city">Bordeaux</settlement>
<region type="region" nuts="2">Nouvelle-Aquitaine</region>
<region type="old region" nuts="2">Aquitaine</region>
</placeName>
<orgName type="university">Université de Bordeaux</orgName>
</affiliation>
</author>
</analytic>
<series><title level="j">Autophagy</title>
<idno type="ISSN">1554-8627</idno>
<imprint><date type="datePub">2016-01-13</date>
</imprint>
</series>
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</sourceDesc>
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<profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>ATP13A2</term>
<term>GBA</term>
<term>Parkinson disease</term>
<term>XMEA</term>
<term>lysosome</term>
<term>nanoparticles</term>
<term>neurodegeneration</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">              <p>Lysosomal impairment causes lysosomal storage disorders (LSD) and is involved in pathogenesis of neurodegenerative diseases, notably Parkinson disease (PD). Strategies enhancing or restoring lysosomal-mediated degradation thus appear as tantalising disease-modifying therapeutics. Here we demonstrate that poly(DL-lactide-co-glycolide) (PLGA) acidic nanoparticles (aNP) restore impaired lysosomal function in a series of toxin and genetic cellular models of PD, i.e. ATP13A2-mutant or depleted cells or glucocerebrosidase (GBA)-mutant cells, as well as in a genetic model of lysosomal-related myopathy. We show that PLGA-aNP are transported to the lysosome within 24 h, lower lysosomal pH and rescue chloroquine (CQ)-induced toxicity. Re-acidification of defective lysosomes following PLGA-aNP treatment restores lysosomal function in different pathological contexts. Finally, our results show that PLGA-aNP may be detected after intracerebral injection in neurons and attenuate PD-related neurodegeneration in vivo by mechanisms involving a rescue of compromised lysosomes.</p>
            </div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
</country>
<region><li>Aquitaine</li>
<li>Nouvelle-Aquitaine</li>
</region>
<settlement><li>Bordeaux</li>
</settlement>
<orgName><li>Université de Bordeaux</li>
</orgName>
</list>
<tree><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Bourdenx, Mathieu" sort="Bourdenx, Mathieu" uniqKey="Bourdenx M" first="Mathieu" last="Bourdenx">Mathieu Bourdenx</name>
</region>
<name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
<name sortKey="Blanchard Desce, Mireille" sort="Blanchard Desce, Mireille" uniqKey="Blanchard Desce M" first="Mireille" last="Blanchard-Desce">Mireille Blanchard-Desce</name>
<name sortKey="Daniel, Jonathan" sort="Daniel, Jonathan" uniqKey="Daniel J" first="Jonathan" last="Daniel">Jonathan Daniel</name>
<name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
<name sortKey="Genin, Emilie" sort="Genin, Emilie" uniqKey="Genin E" first="Emilie" last="Genin">Emilie Genin</name>
<name sortKey="Soria, Federico N" sort="Soria, Federico N" uniqKey="Soria F" first="Federico N" last="Soria">Federico N. Soria</name>
</country>
</tree>
</affiliations>
</record>

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Nanoparticles restore lysosomal acidification defects: Implication for Parkinson and other lysosomal-related diseases.

Nanoparticles restore lysosomal acidification defects: Implication for Parkinson and other lysosomal-related diseases.

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