ParkinsonFranceV1, Main, Curation, bibRecord, 000223

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

Identifieur interne : 000223 ( Main/Curation ); précédent : 000222; suivant : 000224

Nanoparticles restore lysosomal acidification defects: Implications 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.

RBID : PMC:4835967

English descriptors

KwdEn :
- 1-Methyl-4-phenylpyridinium, Acids (metabolism), Alkalies (chemistry), Animals, Cell Death, Dopaminergic Neurons (metabolism), Humans, Hydrogen-Ion Concentration, Injections, Intraventricular, Lactic Acid (chemistry), Lysosomal Storage Diseases (pathology), Lysosomes (metabolism), Lysosomes (ultrastructure), Mice, Models, Biological, Models, Genetic, Nanoparticles (chemistry), Nanoparticles (ultrastructure), Neostriatum (pathology), Nerve Degeneration (pathology), Parkinson Disease (pathology), Polyglycolic Acid (chemistry).
MESH :
- chemical , chemistry : Alkalies, Lactic Acid, Polyglycolic Acid.
- chemical , metabolism : Acids.
- chemical : 1-Methyl-4-phenylpyridinium.
- chemistry : Nanoparticles.
- metabolism : Dopaminergic Neurons, Lysosomes.
- pathology : Lysosomal Storage Diseases, Neostriatum, Nerve Degeneration, Parkinson Disease.
- ultrastructure : Lysosomes, Nanoparticles.
- Animals, Cell Death, Humans, Hydrogen-Ion Concentration, Injections, Intraventricular, Mice, Models, Biological, Models, Genetic.

Abstract

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 tantalizing 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:

DOI: 10.1080/15548627.2015.1136769
PubMed: 26761717
PubMed Central: 4835967

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PMC:4835967

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Nanoparticles restore lysosomal acidification defects: Implication for Parkinson and other lysosomal-related diseases.</title>
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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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<author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
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<author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
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<region type="region" nuts="2">Nouvelle-Aquitaine</region>
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</placeName>
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</author>
</analytic>
<series><title level="j">Autophagy</title>
<idno type="ISSN">1554-8627</idno>
<imprint><date type="datePub">2016-01-13</date>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
</TEI>
</HAL>
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<author><name sortKey="Bourdenx, Mathieu" sort="Bourdenx, Mathieu" uniqKey="Bourdenx M" first="Mathieu" last="Bourdenx">Mathieu Bourdenx</name>
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,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Daniel, Jonathan" sort="Daniel, Jonathan" uniqKey="Daniel J" first="Jonathan" last="Daniel">Jonathan Daniel</name>
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,<addr-line>UMR 5255</addr-line>
, Talence,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Genin, Emilie" sort="Genin, Emilie" uniqKey="Genin E" first="Emilie" last="Genin">Emilie Genin</name>
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,<addr-line>UMR 5255</addr-line>
, Talence,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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</author>
<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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,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
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<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
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, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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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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<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
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,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
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<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<affiliation wicri:level="1"><nlm:aff id="af0001"><institution>University de Bordeaux, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
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<author><name sortKey="Daniel, Jonathan" sort="Daniel, Jonathan" uniqKey="Daniel J" first="Jonathan" last="Daniel">Jonathan Daniel</name>
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,<addr-line>UMR 5255</addr-line>
, Talence,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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</author>
<author><name sortKey="Genin, Emilie" sort="Genin, Emilie" uniqKey="Genin E" first="Emilie" last="Genin">Emilie Genin</name>
<affiliation wicri:level="1"><nlm:aff id="af0003"><institution>University de Bordeaux, Institut des Sciences Moléculaires</institution>
,<addr-line>UMR 5255</addr-line>
, Talence,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Soria, Federico N" sort="Soria, Federico N" uniqKey="Soria F" first="Federico N." last="Soria">Federico N. Soria</name>
<affiliation wicri:level="1"><nlm:aff id="af0001"><institution>University de Bordeaux, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Blanchard Desce, Mireille" sort="Blanchard Desce, Mireille" uniqKey="Blanchard Desce M" first="Mireille" last="Blanchard-Desce">Mireille Blanchard-Desce</name>
<affiliation wicri:level="1"><nlm:aff id="af0003"><institution>University de Bordeaux, Institut des Sciences Moléculaires</institution>
,<addr-line>UMR 5255</addr-line>
, Talence,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
<affiliation wicri:level="1"><nlm:aff id="af0001"><institution>University de Bordeaux, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
<affiliation wicri:level="1"><nlm:aff id="af0001"><institution>University de Bordeaux, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af0002"><institution>CNRS, Institut des Maladies Neurodégénératives</institution>
,<addr-line>UMR 5293</addr-line>
, Bordeaux,<country>France</country>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Autophagy</title>
<idno type="ISSN">1554-8627</idno>
<idno type="eISSN">1554-8635</idno>
<imprint><date when="2016">2016</date>
</imprint>
</series>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenylpyridinium</term>
<term>Acids (metabolism)</term>
<term>Alkalies (chemistry)</term>
<term>Animals</term>
<term>Cell Death</term>
<term>Dopaminergic Neurons (metabolism)</term>
<term>Humans</term>
<term>Hydrogen-Ion Concentration</term>
<term>Injections, Intraventricular</term>
<term>Lactic Acid (chemistry)</term>
<term>Lysosomal Storage Diseases (pathology)</term>
<term>Lysosomes (metabolism)</term>
<term>Lysosomes (ultrastructure)</term>
<term>Mice</term>
<term>Models, Biological</term>
<term>Models, Genetic</term>
<term>Nanoparticles (chemistry)</term>
<term>Nanoparticles (ultrastructure)</term>
<term>Neostriatum (pathology)</term>
<term>Nerve Degeneration (pathology)</term>
<term>Parkinson Disease (pathology)</term>
<term>Polyglycolic Acid (chemistry)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Alkalies</term>
<term>Lactic Acid</term>
<term>Polyglycolic Acid</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Acids</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenylpyridinium</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Nanoparticles</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term>
<term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lysosomal Storage Diseases</term>
<term>Neostriatum</term>
<term>Nerve Degeneration</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Lysosomes</term>
<term>Nanoparticles</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Death</term>
<term>Humans</term>
<term>Hydrogen-Ion Concentration</term>
<term>Injections, Intraventricular</term>
<term>Mice</term>
<term>Models, Biological</term>
<term>Models, Genetic</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><title>ABSTRACT</title>
<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 tantalizing disease-modifying therapeutics. Here we demonstrate that poly(DL-lactide-<italic>co</italic>
-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>
</PMC>
</double>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

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

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

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