Systemic exosomal siRNA delivery reduced alpha-synuclein aggregates in brains of transgenic mice.
Identifieur interne : 000432 ( PubMed/Corpus ); précédent : 000431; suivant : 000433Systemic exosomal siRNA delivery reduced alpha-synuclein aggregates in brains of transgenic mice.
Auteurs : J Mark Cooper ; P B Oscar Wiklander ; Joel Z. Nordin ; Raya Al-Shawi ; Matthew J. Wood ; Mansi Vithlani ; Anthony H V. Schapira ; J Paul Simons ; Samir El-Andaloussi ; Lydia Alvarez-ErvitiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Brain (metabolism), Cell Line, Tumor, Dendritic Cells (metabolism), Exosomes (physiology), Gene Expression Regulation (drug effects), Gene Expression Regulation (physiology), Genetic Vectors (genetics), Glycoproteins (administration & dosage), Glycoproteins (genetics), Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mutation (genetics), Neuroblastoma (pathology), Peptide Fragments (administration & dosage), Peptide Fragments (genetics), RNA, Messenger (metabolism), RNA, Small Interfering (administration & dosage), Time Factors, Transfection, Viral Proteins (administration & dosage), Viral Proteins (genetics), alpha-Synuclein (genetics), alpha-Synuclein (metabolism).
- MESH :
- chemical , administration & dosage : Glycoproteins, Peptide Fragments, RNA, Small Interfering, Viral Proteins.
- drug effects : Gene Expression Regulation.
- genetics : Genetic Vectors, Glycoproteins, Mutation, Peptide Fragments, Viral Proteins, alpha-Synuclein.
- metabolism : Brain, Dendritic Cells, RNA, Messenger, alpha-Synuclein.
- pathology : Neuroblastoma.
- physiology : Exosomes, Gene Expression Regulation.
- Animals, Cell Line, Tumor, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Time Factors, Transfection.
Abstract
Alpha-synuclein (α-Syn) aggregates are the main component of Lewy bodies, which are the characteristic pathological feature in Parkinson's disease (PD) brain. Evidence that α-Syn aggregation can be propagated between neurones has led to the suggestion that this mechanism is responsible for the stepwise progression of PD pathology. Decreasing α-Syn expression is predicted to attenuate this process and is thus an attractive approach to delay or halt PD progression. We have used α-Syn small interfering RNA (siRNA) to reduce total and aggregated α-Syn levels in mouse brains. To achieve widespread delivery of siRNAs to the brain we have peripherally injected modified exosomes expressing Ravies virus glycoprotein loaded with siRNA. Normal mice were analyzed 3 or 7 days after injection. To evaluate whether this approach can decrease α-Syn aggregates, we repeated the treatment using transgenic mice expressing the human phosphorylation-mimic S129D α-Syn, which exhibits aggregation. In normal mice we detected significantly reduced α-Syn messenger RNA (mRNA) and protein levels throughout the brain 3 and 7 days after treatment with RVG-exosomes loaded with siRNA to α-Syn. In S129D α-Syn transgenic mice we found a decreased α-Syn mRNA and protein levels throughout the brain 7 days after injection. This resulted in significant reductions in intraneuronal protein aggregates, including in dopaminergic neurones of the substantia nigra. This study highlights the therapeutic potential of RVG-exosome delivery of siRNA to delay and reverse brain α-Syn pathological conditions.
DOI: 10.1002/mds.25978
PubMed: 25112864
Links to Exploration step
pubmed:25112864Le document en format XML
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Nordin</name></author><author><name sortKey="Al Shawi, Raya" sort="Al Shawi, Raya" uniqKey="Al Shawi R" first="Raya" last="Al-Shawi">Raya Al-Shawi</name></author><author><name sortKey="Wood, Matthew J" sort="Wood, Matthew J" uniqKey="Wood M" first="Matthew J" last="Wood">Matthew J. Wood</name></author><author><name sortKey="Vithlani, Mansi" sort="Vithlani, Mansi" uniqKey="Vithlani M" first="Mansi" last="Vithlani">Mansi Vithlani</name></author><author><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H V" last="Schapira">Anthony H V. 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Nordin</name></author><author><name sortKey="Al Shawi, Raya" sort="Al Shawi, Raya" uniqKey="Al Shawi R" first="Raya" last="Al-Shawi">Raya Al-Shawi</name></author><author><name sortKey="Wood, Matthew J" sort="Wood, Matthew J" uniqKey="Wood M" first="Matthew J" last="Wood">Matthew J. Wood</name></author><author><name sortKey="Vithlani, Mansi" sort="Vithlani, Mansi" uniqKey="Vithlani M" first="Mansi" last="Vithlani">Mansi Vithlani</name></author><author><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H V" last="Schapira">Anthony H V. Schapira</name></author><author><name sortKey="Simons, J Paul" sort="Simons, J Paul" uniqKey="Simons J" first="J Paul" last="Simons">J Paul Simons</name></author><author><name sortKey="El Andaloussi, Samir" sort="El Andaloussi, Samir" uniqKey="El Andaloussi S" first="Samir" last="El-Andaloussi">Samir El-Andaloussi</name></author><author><name sortKey="Alvarez Erviti, Lydia" sort="Alvarez Erviti, Lydia" uniqKey="Alvarez Erviti L" first="Lydia" last="Alvarez-Erviti">Lydia Alvarez-Erviti</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</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>Brain (metabolism)</term><term>Cell Line, Tumor</term><term>Dendritic Cells (metabolism)</term><term>Exosomes (physiology)</term><term>Gene Expression Regulation (drug effects)</term><term>Gene Expression Regulation (physiology)</term><term>Genetic Vectors (genetics)</term><term>Glycoproteins (administration & dosage)</term><term>Glycoproteins (genetics)</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Mutation (genetics)</term><term>Neuroblastoma (pathology)</term><term>Peptide Fragments (administration & dosage)</term><term>Peptide Fragments (genetics)</term><term>RNA, Messenger (metabolism)</term><term>RNA, Small Interfering (administration & dosage)</term><term>Time Factors</term><term>Transfection</term><term>Viral Proteins (administration & dosage)</term><term>Viral Proteins (genetics)</term><term>alpha-Synuclein (genetics)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Glycoproteins</term><term>Peptide Fragments</term><term>RNA, Small Interfering</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genetic Vectors</term><term>Glycoproteins</term><term>Mutation</term><term>Peptide Fragments</term><term>Viral Proteins</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Dendritic Cells</term><term>RNA, Messenger</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neuroblastoma</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Exosomes</term><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Time Factors</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alpha-synuclein (α-Syn) aggregates are the main component of Lewy bodies, which are the characteristic pathological feature in Parkinson's disease (PD) brain. Evidence that α-Syn aggregation can be propagated between neurones has led to the suggestion that this mechanism is responsible for the stepwise progression of PD pathology. Decreasing α-Syn expression is predicted to attenuate this process and is thus an attractive approach to delay or halt PD progression. We have used α-Syn small interfering RNA (siRNA) to reduce total and aggregated α-Syn levels in mouse brains. To achieve widespread delivery of siRNAs to the brain we have peripherally injected modified exosomes expressing Ravies virus glycoprotein loaded with siRNA. Normal mice were analyzed 3 or 7 days after injection. To evaluate whether this approach can decrease α-Syn aggregates, we repeated the treatment using transgenic mice expressing the human phosphorylation-mimic S129D α-Syn, which exhibits aggregation. In normal mice we detected significantly reduced α-Syn messenger RNA (mRNA) and protein levels throughout the brain 3 and 7 days after treatment with RVG-exosomes loaded with siRNA to α-Syn. In S129D α-Syn transgenic mice we found a decreased α-Syn mRNA and protein levels throughout the brain 7 days after injection. This resulted in significant reductions in intraneuronal protein aggregates, including in dopaminergic neurones of the substantia nigra. This study highlights the therapeutic potential of RVG-exosome delivery of siRNA to delay and reverse brain α-Syn pathological conditions.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">25112864</PMID><DateCreated><Year>2014</Year><Month>10</Month><Day>06</Day></DateCreated><DateCompleted><Year>2015</Year><Month>06</Month><Day>03</Day></DateCompleted><DateRevised><Year>2015</Year><Month>01</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>12</Issue><PubDate><Year>2014</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Systemic exosomal siRNA delivery reduced alpha-synuclein aggregates in brains of transgenic mice.</ArticleTitle><Pagination><MedlinePgn>1476-85</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25978</ELocationID><Abstract><AbstractText>Alpha-synuclein (α-Syn) aggregates are the main component of Lewy bodies, which are the characteristic pathological feature in Parkinson's disease (PD) brain. Evidence that α-Syn aggregation can be propagated between neurones has led to the suggestion that this mechanism is responsible for the stepwise progression of PD pathology. Decreasing α-Syn expression is predicted to attenuate this process and is thus an attractive approach to delay or halt PD progression. We have used α-Syn small interfering RNA (siRNA) to reduce total and aggregated α-Syn levels in mouse brains. To achieve widespread delivery of siRNAs to the brain we have peripherally injected modified exosomes expressing Ravies virus glycoprotein loaded with siRNA. Normal mice were analyzed 3 or 7 days after injection. To evaluate whether this approach can decrease α-Syn aggregates, we repeated the treatment using transgenic mice expressing the human phosphorylation-mimic S129D α-Syn, which exhibits aggregation. In normal mice we detected significantly reduced α-Syn messenger RNA (mRNA) and protein levels throughout the brain 3 and 7 days after treatment with RVG-exosomes loaded with siRNA to α-Syn. In S129D α-Syn transgenic mice we found a decreased α-Syn mRNA and protein levels throughout the brain 7 days after injection. This resulted in significant reductions in intraneuronal protein aggregates, including in dopaminergic neurones of the substantia nigra. This study highlights the therapeutic potential of RVG-exosome delivery of siRNA to delay and reverse brain α-Syn pathological conditions.</AbstractText><CopyrightInformation>© 2014 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cooper</LastName><ForeName>J Mark</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Clinical Neuroscience, Institute of Neurology, University College London, London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wiklander</LastName><ForeName>P B Oscar</ForeName><Initials>PB</Initials></Author><Author ValidYN="Y"><LastName>Nordin</LastName><ForeName>Joel Z</ForeName><Initials>JZ</Initials></Author><Author ValidYN="Y"><LastName>Al-Shawi</LastName><ForeName>Raya</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Wood</LastName><ForeName>Matthew J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Vithlani</LastName><ForeName>Mansi</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Schapira</LastName><ForeName>Anthony H V</ForeName><Initials>AH</Initials></Author><Author ValidYN="Y"><LastName>Simons</LastName><ForeName>J Paul</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>El-Andaloussi</LastName><ForeName>Samir</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Alvarez-Erviti</LastName><ForeName>Lydia</ForeName><Initials>L</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>089698</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>F-1101</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G-0910</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G-1109</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MR/J009660/1</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>WT089698</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><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>08</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006023">Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010446">Peptide Fragments</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C583075">rabies virus glycoprotein peptide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2014 Mar;75(3):351-62</RefSource><PMID 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