Nanoparticles restore lysosomal acidification defects: Implications for Parkinson and other lysosomal-related diseases.
Identifieur interne : 000212 ( PubMed/Corpus ); précédent : 000211; suivant : 000213Nanoparticles restore lysosomal acidification defects: Implications for Parkinson and other lysosomal-related diseases.
Auteurs : Mathieu Bourdenx ; Jonathan Daniel ; Emilie Genin ; Federico N. Soria ; Mireille Blanchard-Desce ; Erwan Bezard ; Benjamin DehaySource :
- Autophagy [ 1554-8635 ] ; 2016.
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
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.
DOI: 10.1080/15548627.2015.1136769
PubMed: 26761717
Links to Exploration step
pubmed:26761717Le document en format XML
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Soria</name><affiliation><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></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><nlm:affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</nlm:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></affiliation></author><author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name><affiliation><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26761717</idno><idno type="pmid">26761717</idno><idno type="doi">10.1080/15548627.2015.1136769</idno><idno type="wicri:Area/PubMed/Corpus">000212</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000212</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Nanoparticles restore lysosomal acidification defects: Implications for Parkinson and other lysosomal-related diseases.</title><author><name sortKey="Bourdenx, Mathieu" sort="Bourdenx, Mathieu" uniqKey="Bourdenx M" first="Mathieu" last="Bourdenx">Mathieu Bourdenx</name><affiliation><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></affiliation></author><author><name sortKey="Daniel, Jonathan" sort="Daniel, Jonathan" uniqKey="Daniel J" first="Jonathan" last="Daniel">Jonathan Daniel</name><affiliation><nlm:affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</nlm:affiliation></affiliation></author><author><name sortKey="Genin, Emilie" sort="Genin, Emilie" uniqKey="Genin E" first="Emilie" last="Genin">Emilie Genin</name><affiliation><nlm:affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</nlm:affiliation></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><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></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><nlm:affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</nlm:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></affiliation></author><author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name><affiliation><nlm:affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><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">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26761717</PMID><DateCreated><Year>2016</Year><Month>04</Month><Day>06</Day></DateCreated><DateCompleted><Year>2016</Year><Month>12</Month><Day>26</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>3</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>Nanoparticles restore lysosomal acidification defects: Implications for Parkinson and other lysosomal-related diseases.</ArticleTitle><Pagination><MedlinePgn>472-83</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2015.1136769</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bourdenx</LastName><ForeName>Mathieu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b CNRS, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Daniel</LastName><ForeName>Jonathan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Genin</LastName><ForeName>Emilie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soria</LastName><ForeName>Federico N</ForeName><Initials>FN</Initials><AffiliationInfo><Affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b CNRS, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blanchard-Desce</LastName><ForeName>Mireille</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>c University de Bordeaux, Institut des Sciences Moléculaires , UMR 5255, Talence , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>Erwan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b CNRS, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dehay</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>a University de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b CNRS, Institut des Maladies Neurodégénératives , UMR 5293, Bordeaux , France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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MajorTopicYN="N">neurodegeneration</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>1</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>1</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>12</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26761717</ArticleId><ArticleId IdType="doi">10.1080/15548627.2015.1136769</ArticleId><ArticleId IdType="pmc">PMC4835967</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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