Major Alterations of Phosphatidylcholine and Lysophosphotidylcholine Lipids in the Substantia Nigra Using an Early Stage Model of Parkinson's Disease.
Identifieur interne : 000473 ( PubMed/Checkpoint ); précédent : 000472; suivant : 000474Major Alterations of Phosphatidylcholine and Lysophosphotidylcholine Lipids in the Substantia Nigra Using an Early Stage Model of Parkinson's Disease.
Auteurs : Kyle Farmer [Canada] ; Catherine A. Smith [Canada] ; Shawn Hayley [Canada] ; Jeffrey Smith [Canada]Source :
- International journal of molecular sciences [ 1422-0067 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Lysophosphatidylcholines, Phosphatidylcholines.
- metabolism : Parkinson Disease, Substantia Nigra.
- Animals, Disease Models, Animal, Humans, Lipid Metabolism, Male, Rats, Tandem Mass Spectrometry.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disease affecting the nigrostriatal pathway, where patients do not manifest motor symptoms until >50% of neurons are lost. Thus, it is of great importance to determine early neuronal changes that may contribute to disease progression. Recent attention has focused on lipids and their role in pro- and anti-apoptotic processes. However, information regarding the lipid alterations in animal models of PD is lacking. In this study, we utilized high performance liquid chromatography electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) and novel HPLC solvent methodology to profile phosphatidylcholines and sphingolipids within the substantia nigra. The ipsilateral substantia nigra pars compacta was collected from rats 21 days after an infusion of 6-hydroxydopamine (6-OHDA), or vehicle into the anterior dorsal striatum. We identified 115 lipid species from their mass/charge ratio using the LMAPS Lipid MS Predict Database. Of these, 19 lipid species (from phosphatidylcholine and lysophosphotidylcholine lipid classes) were significantly altered by 6-OHDA, with most being down-regulated. The two lipid species that were up-regulated were LPC (16:0) and LPC (18:1), which are important for neuroinflammatory signalling. These findings provide a first step in the characterization of lipid changes in early stages of PD-like pathology and could provide novel targets for early interventions in PD.
DOI: 10.3390/ijms160818865
PubMed: 26274953
Affiliations:
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Smith</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. csmith@connect.carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author><author><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. shawn_hayley@carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author><author><name sortKey="Smith, Jeffrey" sort="Smith, Jeffrey" uniqKey="Smith J" first="Jeffrey" last="Smith">Jeffrey Smith</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Chemistry and Institute of Biochemistry, 1125 Colonel By Drive, Steacie Building, Ottawa, ON K1S 5B6, Canada. jeff_smith@carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Chemistry and Institute of Biochemistry, 1125 Colonel By Drive, Steacie Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26274953</idno><idno type="pmid">26274953</idno><idno type="doi">10.3390/ijms160818865</idno><idno type="wicri:Area/PubMed/Corpus">000441</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000441</idno><idno type="wicri:Area/PubMed/Curation">000441</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000441</idno><idno type="wicri:Area/PubMed/Checkpoint">000441</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000441</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Major Alterations of Phosphatidylcholine and Lysophosphotidylcholine Lipids in the Substantia Nigra Using an Early Stage Model of Parkinson's Disease.</title><author><name sortKey="Farmer, Kyle" sort="Farmer, Kyle" uniqKey="Farmer K" first="Kyle" last="Farmer">Kyle Farmer</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. kyle_farmer@carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author><author><name sortKey="Smith, Catherine A" sort="Smith, Catherine A" uniqKey="Smith C" first="Catherine A" last="Smith">Catherine A. Smith</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. csmith@connect.carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author><author><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. shawn_hayley@carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author><author><name sortKey="Smith, Jeffrey" sort="Smith, Jeffrey" uniqKey="Smith J" first="Jeffrey" last="Smith">Jeffrey Smith</name><affiliation wicri:level="1"><nlm:affiliation>Carleton University Department of Chemistry and Institute of Biochemistry, 1125 Colonel By Drive, Steacie Building, Ottawa, ON K1S 5B6, Canada. jeff_smith@carleton.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Carleton University Department of Chemistry and Institute of Biochemistry, 1125 Colonel By Drive, Steacie Building, Ottawa, ON K1S 5B6</wicri:regionArea><wicri:noRegion>ON K1S 5B6</wicri:noRegion></affiliation></author></analytic><series><title level="j">International journal of molecular sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Lipid Metabolism</term><term>Lysophosphatidylcholines (metabolism)</term><term>Male</term><term>Parkinson Disease (metabolism)</term><term>Phosphatidylcholines (metabolism)</term><term>Rats</term><term>Substantia Nigra (metabolism)</term><term>Tandem Mass Spectrometry</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Lysophosphatidylcholines</term><term>Phosphatidylcholines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Lipid Metabolism</term><term>Male</term><term>Rats</term><term>Tandem Mass Spectrometry</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive neurodegenerative disease affecting the nigrostriatal pathway, where patients do not manifest motor symptoms until >50% of neurons are lost. Thus, it is of great importance to determine early neuronal changes that may contribute to disease progression. Recent attention has focused on lipids and their role in pro- and anti-apoptotic processes. However, information regarding the lipid alterations in animal models of PD is lacking. In this study, we utilized high performance liquid chromatography electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) and novel HPLC solvent methodology to profile phosphatidylcholines and sphingolipids within the substantia nigra. The ipsilateral substantia nigra pars compacta was collected from rats 21 days after an infusion of 6-hydroxydopamine (6-OHDA), or vehicle into the anterior dorsal striatum. We identified 115 lipid species from their mass/charge ratio using the LMAPS Lipid MS Predict Database. Of these, 19 lipid species (from phosphatidylcholine and lysophosphotidylcholine lipid classes) were significantly altered by 6-OHDA, with most being down-regulated. The two lipid species that were up-regulated were LPC (16:0) and LPC (18:1), which are important for neuroinflammatory signalling. These findings provide a first step in the characterization of lipid changes in early stages of PD-like pathology and could provide novel targets for early interventions in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26274953</PMID><DateCreated><Year>2015</Year><Month>08</Month><Day>15</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>10</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><Issue>8</Issue><PubDate><Year>2015</Year><Month>Aug</Month><Day>12</Day></PubDate></JournalIssue><Title>International journal of molecular sciences</Title><ISOAbbreviation>Int J Mol Sci</ISOAbbreviation></Journal><ArticleTitle>Major Alterations of Phosphatidylcholine and Lysophosphotidylcholine Lipids in the Substantia Nigra Using an Early Stage Model of Parkinson's Disease.</ArticleTitle><Pagination><MedlinePgn>18865-77</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3390/ijms160818865</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a progressive neurodegenerative disease affecting the nigrostriatal pathway, where patients do not manifest motor symptoms until >50% of neurons are lost. Thus, it is of great importance to determine early neuronal changes that may contribute to disease progression. Recent attention has focused on lipids and their role in pro- and anti-apoptotic processes. However, information regarding the lipid alterations in animal models of PD is lacking. In this study, we utilized high performance liquid chromatography electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) and novel HPLC solvent methodology to profile phosphatidylcholines and sphingolipids within the substantia nigra. The ipsilateral substantia nigra pars compacta was collected from rats 21 days after an infusion of 6-hydroxydopamine (6-OHDA), or vehicle into the anterior dorsal striatum. We identified 115 lipid species from their mass/charge ratio using the LMAPS Lipid MS Predict Database. Of these, 19 lipid species (from phosphatidylcholine and lysophosphotidylcholine lipid classes) were significantly altered by 6-OHDA, with most being down-regulated. The two lipid species that were up-regulated were LPC (16:0) and LPC (18:1), which are important for neuroinflammatory signalling. These findings provide a first step in the characterization of lipid changes in early stages of PD-like pathology and could provide novel targets for early interventions in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Farmer</LastName><ForeName>Kyle</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. kyle_farmer@carleton.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>Catherine A</ForeName><Initials>CA</Initials><AffiliationInfo><Affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. csmith@connect.carleton.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hayley</LastName><ForeName>Shawn</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Carleton University Department of Neuroscience, 1125 Colonel By Drive, Life Sciences Research Building, Ottawa, ON K1S 5B6, Canada. shawn_hayley@carleton.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>Jeffrey</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Carleton University Department of Chemistry and Institute of Biochemistry, 1125 Colonel By Drive, Steacie Building, Ottawa, ON K1S 5B6, Canada. jeff_smith@carleton.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</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>2015</Year><Month>08</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Int J Mol Sci</MedlineTA><NlmUniqueID>101092791</NlmUniqueID><ISSNLinking>1422-0067</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008244">Lysophosphatidylcholines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010713">Phosphatidylcholines</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2008;14 Suppl 2:S124-9</RefSource><PMID Version="1">18595767</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Traffic. 2011 Sep;12(9):1257-68</RefSource><PMID Version="1">21649806</PMID></CommentsCorrections><CommentsCorrections 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MajorTopicYN="N">lipidomic profile</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>06</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>08</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>08</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>8</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>8</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>5</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26274953</ArticleId><ArticleId IdType="pii">ijms160818865</ArticleId><ArticleId IdType="doi">10.3390/ijms160818865</ArticleId><ArticleId IdType="pmc">PMC4581276</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Farmer, Kyle" sort="Farmer, Kyle" uniqKey="Farmer K" first="Kyle" last="Farmer">Kyle Farmer</name></noRegion><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><name sortKey="Smith, Catherine A" sort="Smith, Catherine A" uniqKey="Smith C" first="Catherine A" last="Smith">Catherine A. Smith</name><name sortKey="Smith, Jeffrey" sort="Smith, Jeffrey" uniqKey="Smith J" first="Jeffrey" last="Smith">Jeffrey Smith</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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