Progranulin gene delivery protects dopaminergic neurons in a mouse model of Parkinson's disease.
Identifieur interne : 000672 ( PubMed/Checkpoint ); précédent : 000671; suivant : 000673Progranulin gene delivery protects dopaminergic neurons in a mouse model of Parkinson's disease.
Auteurs : Jackalina M. Van Kampen [Canada] ; David Baranowski [Canada] ; Denis G. Kay [Canada]Source :
- PloS one [ 1932-6203 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Apoptosis (genetics), Disease Models, Animal, Dopamine (genetics), Dopamine (metabolism), Dopaminergic Neurons (metabolism), Dopaminergic Neurons (pathology), Gene Transfer Techniques, Genetic Therapy, Humans, Intercellular Signaling Peptides and Proteins (biosynthesis), Intercellular Signaling Peptides and Proteins (genetics), MPTP Poisoning (drug therapy), MPTP Poisoning (genetics), MPTP Poisoning (pathology), Mice, Motor Activity (drug effects), Motor Activity (immunology), Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson Disease (pathology).
- MESH :
- chemical , biosynthesis : Intercellular Signaling Peptides and Proteins.
- chemical , genetics : Dopamine, Intercellular Signaling Peptides and Proteins.
- drug effects : Motor Activity.
- drug therapy : MPTP Poisoning, Parkinson Disease.
- genetics : Apoptosis, MPTP Poisoning, Parkinson Disease.
- immunology : Motor Activity.
- chemical , metabolism : Dopamine, Dopaminergic Neurons.
- pathology : Dopaminergic Neurons, MPTP Poisoning, Parkinson Disease.
- Animals, Disease Models, Animal, Gene Transfer Techniques, Genetic Therapy, Humans, Mice.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by tremor, rigidity and akinesia/bradykinesia resulting from the progressive loss of nigrostriatal dopaminergic neurons. To date, only symptomatic treatment is available for PD patients, with no effective means of slowing or stopping the progression of the disease. Progranulin (PGRN) is a 593 amino acid multifunction protein that is widely distributed throughout the CNS, localized primarily in neurons and microglia. PGRN has been demonstrated to be a potent regulator of neuroinflammation and also acts as an autocrine neurotrophic factor, important for long-term neuronal survival. Thus, enhancing PGRN expression may strengthen the cells resistance to disease. In the present study, we have used the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate the possible use of PGRN gene delivery as a therapy for the prevention or treatment of PD. Viral vector delivery of the PGRN gene was an effective means of elevating PGRN expression in nigrostriatal neurons. When PGRN expression was elevated in the SNC, nigrostriatal neurons were protected from MPTP toxicity in mice, along with a preservation of striatal dopamine content and turnover. Further, protection of nigrostriatal neurons by PGRN gene therapy was accompanied by reductions in markers of MPTP-induced inflammation and apoptosis as well as a complete preservation of locomotor function. We conclude that PGRN gene therapy may have beneficial effects in the treatment of PD.
DOI: 10.1371/journal.pone.0097032
PubMed: 24804730
Affiliations:
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Van Kampen</name><affiliation wicri:level="1"><nlm:affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Biomedical Science, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Biomedical Science, University of Prince Edward Island, Charlottetown, Prince Edward Island</wicri:regionArea><wicri:noRegion>Prince Edward Island</wicri:noRegion></affiliation></author><author><name sortKey="Baranowski, David" sort="Baranowski, David" uniqKey="Baranowski D" first="David" last="Baranowski">David Baranowski</name><affiliation wicri:level="1"><nlm:affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodyn Inc., Charlottetown, Prince Edward Island</wicri:regionArea><wicri:noRegion>Prince Edward Island</wicri:noRegion></affiliation></author><author><name sortKey="Kay, Denis G" sort="Kay, Denis G" uniqKey="Kay D" first="Denis G" last="Kay">Denis G. Kay</name><affiliation wicri:level="1"><nlm:affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Pathology and Microbiology, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Pathology and Microbiology, University of Prince Edward Island, Charlottetown, Prince Edward Island</wicri:regionArea><wicri:noRegion>Prince Edward Island</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24804730</idno><idno type="pmid">24804730</idno><idno type="doi">10.1371/journal.pone.0097032</idno><idno type="wicri:Area/PubMed/Corpus">000752</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000752</idno><idno type="wicri:Area/PubMed/Curation">000752</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000752</idno><idno type="wicri:Area/PubMed/Checkpoint">000752</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000752</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Progranulin gene delivery protects dopaminergic neurons in a mouse model of Parkinson's disease.</title><author><name sortKey="Van Kampen, Jackalina M" sort="Van Kampen, Jackalina M" uniqKey="Van Kampen J" first="Jackalina M" last="Van Kampen">Jackalina M. Van Kampen</name><affiliation wicri:level="1"><nlm:affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Biomedical Science, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Biomedical Science, University of Prince Edward Island, Charlottetown, Prince Edward Island</wicri:regionArea><wicri:noRegion>Prince Edward Island</wicri:noRegion></affiliation></author><author><name sortKey="Baranowski, David" sort="Baranowski, David" uniqKey="Baranowski D" first="David" last="Baranowski">David Baranowski</name><affiliation wicri:level="1"><nlm:affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodyn Inc., Charlottetown, Prince Edward Island</wicri:regionArea><wicri:noRegion>Prince Edward Island</wicri:noRegion></affiliation></author><author><name sortKey="Kay, Denis G" sort="Kay, Denis G" uniqKey="Kay D" first="Denis G" last="Kay">Denis G. Kay</name><affiliation wicri:level="1"><nlm:affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Pathology and Microbiology, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Pathology and Microbiology, University of Prince Edward Island, Charlottetown, Prince Edward Island</wicri:regionArea><wicri:noRegion>Prince Edward Island</wicri:noRegion></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis (genetics)</term><term>Disease Models, Animal</term><term>Dopamine (genetics)</term><term>Dopamine (metabolism)</term><term>Dopaminergic Neurons (metabolism)</term><term>Dopaminergic Neurons (pathology)</term><term>Gene Transfer Techniques</term><term>Genetic Therapy</term><term>Humans</term><term>Intercellular Signaling Peptides and Proteins (biosynthesis)</term><term>Intercellular Signaling Peptides and Proteins (genetics)</term><term>MPTP Poisoning (drug therapy)</term><term>MPTP Poisoning (genetics)</term><term>MPTP Poisoning (pathology)</term><term>Mice</term><term>Motor Activity (drug effects)</term><term>Motor Activity (immunology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Intercellular Signaling Peptides and Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dopamine</term><term>Intercellular Signaling Peptides and Proteins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>MPTP Poisoning</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term><term>MPTP Poisoning</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Dopaminergic Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dopaminergic Neurons</term><term>MPTP Poisoning</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Gene Transfer Techniques</term><term>Genetic Therapy</term><term>Humans</term><term>Mice</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by tremor, rigidity and akinesia/bradykinesia resulting from the progressive loss of nigrostriatal dopaminergic neurons. To date, only symptomatic treatment is available for PD patients, with no effective means of slowing or stopping the progression of the disease. Progranulin (PGRN) is a 593 amino acid multifunction protein that is widely distributed throughout the CNS, localized primarily in neurons and microglia. PGRN has been demonstrated to be a potent regulator of neuroinflammation and also acts as an autocrine neurotrophic factor, important for long-term neuronal survival. Thus, enhancing PGRN expression may strengthen the cells resistance to disease. In the present study, we have used the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate the possible use of PGRN gene delivery as a therapy for the prevention or treatment of PD. Viral vector delivery of the PGRN gene was an effective means of elevating PGRN expression in nigrostriatal neurons. When PGRN expression was elevated in the SNC, nigrostriatal neurons were protected from MPTP toxicity in mice, along with a preservation of striatal dopamine content and turnover. Further, protection of nigrostriatal neurons by PGRN gene therapy was accompanied by reductions in markers of MPTP-induced inflammation and apoptosis as well as a complete preservation of locomotor function. We conclude that PGRN gene therapy may have beneficial effects in the treatment of PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24804730</PMID><DateCreated><Year>2014</Year><Month>05</Month><Day>08</Day></DateCreated><DateCompleted><Year>2015</Year><Month>06</Month><Day>16</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>5</Issue><PubDate><Year>2014</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Progranulin gene delivery protects dopaminergic neurons in a mouse model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>e97032</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0097032</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by tremor, rigidity and akinesia/bradykinesia resulting from the progressive loss of nigrostriatal dopaminergic neurons. To date, only symptomatic treatment is available for PD patients, with no effective means of slowing or stopping the progression of the disease. Progranulin (PGRN) is a 593 amino acid multifunction protein that is widely distributed throughout the CNS, localized primarily in neurons and microglia. PGRN has been demonstrated to be a potent regulator of neuroinflammation and also acts as an autocrine neurotrophic factor, important for long-term neuronal survival. Thus, enhancing PGRN expression may strengthen the cells resistance to disease. In the present study, we have used the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate the possible use of PGRN gene delivery as a therapy for the prevention or treatment of PD. Viral vector delivery of the PGRN gene was an effective means of elevating PGRN expression in nigrostriatal neurons. When PGRN expression was elevated in the SNC, nigrostriatal neurons were protected from MPTP toxicity in mice, along with a preservation of striatal dopamine content and turnover. Further, protection of nigrostriatal neurons by PGRN gene therapy was accompanied by reductions in markers of MPTP-induced inflammation and apoptosis as well as a complete preservation of locomotor function. We conclude that PGRN gene therapy may have beneficial effects in the treatment of PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Van Kampen</LastName><ForeName>Jackalina M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Biomedical Science, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baranowski</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kay</LastName><ForeName>Denis G</ForeName><Initials>DG</Initials><AffiliationInfo><Affiliation>Neurodyn Inc., Charlottetown, Prince Edward Island, Canada; Department of Pathology and Microbiology, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>05</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C120204">Grn protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036341">Intercellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance 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Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4013129</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>02</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>04</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>5</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>5</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>6</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24804730</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0097032</ArticleId><ArticleId IdType="pii">PONE-D-14-08798</ArticleId><ArticleId IdType="pmc">PMC4013129</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Van Kampen, Jackalina M" sort="Van Kampen, Jackalina M" uniqKey="Van Kampen J" first="Jackalina M" last="Van Kampen">Jackalina M. Van Kampen</name></noRegion><name sortKey="Baranowski, David" sort="Baranowski, David" uniqKey="Baranowski D" first="David" last="Baranowski">David Baranowski</name><name sortKey="Kay, Denis G" sort="Kay, Denis G" uniqKey="Kay D" first="Denis G" last="Kay">Denis G. Kay</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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