Transcriptional profile of Parkinson blood mononuclear cells with LRRK2 mutation.
Identifieur interne : 000944 ( PubMed/Corpus ); précédent : 000943; suivant : 000945Transcriptional profile of Parkinson blood mononuclear cells with LRRK2 mutation.
Auteurs : Eugénie Mutez ; Lydie Larvor ; Frédéric Leprêtre ; Vincent Mouroux ; Dorota Hamalek ; Jean-Pierre Kerckaert ; Jordi Pérez-Tur ; Nawal Waucquier ; Christel Vanbesien-Mailliot ; Aurélie Duflot ; David Devos ; Luc Defebvre ; Alexandre Kreisler ; Bernard Frigard ; Alain Destée ; Marie-Christine Chartier-HarlinSource :
- Neurobiology of aging [ 1558-1497 ] ; 2011.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Cell Adhesion Molecules, Neuronal (genetics), Female, Gene Expression Profiling (methods), Humans, Leukocytes, Mononuclear (metabolism), Male, Middle Aged, Mutation (genetics), Oligonucleotide Array Sequence Analysis (methods), Parkinson Disease (genetics), Parkinson Disease (pathology), Principal Component Analysis, Signal Transduction (genetics), Statistics as Topic, Transcription Factors (genetics), Transcription Factors (metabolism), Young Adult.
- MESH :
- chemical , genetics : Cell Adhesion Molecules, Neuronal, Transcription Factors.
- genetics : Mutation, Parkinson Disease, Signal Transduction.
- metabolism : Leukocytes, Mononuclear, Transcription Factors.
- methods : Gene Expression Profiling, Oligonucleotide Array Sequence Analysis.
- pathology : Parkinson Disease.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Principal Component Analysis, Statistics as Topic, Young Adult.
Abstract
To gain insight into systemic molecular events associated with an age-related neurodegenerative disorder, we compared gene expression patterns in peripheral blood mononuclear cells (PBMCs) sampled from elderly, healthy controls and from Parkinson's disease (PD) patients carrying the most frequently found mutation of the LRRK2 gene (G2019S). A transcriptomic approach enabled us to detect differentially expressed genes and revealed perturbations of pathways known to be involved in PD-related neurodegeneration: the ubiquitin-proteasome system, the mitochondrial oxidation system, inflammation, axonal guidance, calcium signalling and apoptosis. Moreover, alterations of the MAP kinase pathway, the actin cytoskeleton, the ephrin receptor system and vesicular transport - all recently associated with the LRRK2 G2019S mutation pathogenesis - were noted. Furthermore, we acquired new evidences of dysregulation in leukocyte extravasation signalling and immune system pathways in PD. These data show that the G2019S mutation affects the entire body and highlight some of the molecular events observed in the brain. This PBMC transcriptomic approach could be used to better understand neurodegeneration in PD and decipher new pathogenetic mechanisms, even at early stages of the disease.
DOI: 10.1016/j.neurobiolaging.2009.10.016
PubMed: 20096956
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Mouroux</name></author><author><name sortKey="Hamalek, Dorota" sort="Hamalek, Dorota" uniqKey="Hamalek D" first="Dorota" last="Hamalek">Dorota Hamalek</name></author><author><name sortKey="Kerckaert, Jean Pierre" sort="Kerckaert, Jean Pierre" uniqKey="Kerckaert J" first="Jean-Pierre" last="Kerckaert">Jean-Pierre Kerckaert</name></author><author><name sortKey="Perez Tur, Jordi" sort="Perez Tur, Jordi" uniqKey="Perez Tur J" first="Jordi" last="Pérez-Tur">Jordi Pérez-Tur</name></author><author><name sortKey="Waucquier, Nawal" sort="Waucquier, Nawal" uniqKey="Waucquier N" first="Nawal" last="Waucquier">Nawal Waucquier</name></author><author><name sortKey="Vanbesien Mailliot, Christel" sort="Vanbesien Mailliot, Christel" uniqKey="Vanbesien Mailliot C" first="Christel" last="Vanbesien-Mailliot">Christel Vanbesien-Mailliot</name></author><author><name sortKey="Duflot, Aurelie" sort="Duflot, Aurelie" uniqKey="Duflot A" first="Aurélie" last="Duflot">Aurélie Duflot</name></author><author><name sortKey="Devos, David" sort="Devos, David" uniqKey="Devos D" first="David" last="Devos">David Devos</name></author><author><name sortKey="Defebvre, Luc" sort="Defebvre, Luc" uniqKey="Defebvre L" first="Luc" last="Defebvre">Luc Defebvre</name></author><author><name sortKey="Kreisler, Alexandre" sort="Kreisler, Alexandre" uniqKey="Kreisler A" first="Alexandre" last="Kreisler">Alexandre Kreisler</name></author><author><name sortKey="Frigard, Bernard" sort="Frigard, Bernard" uniqKey="Frigard B" first="Bernard" last="Frigard">Bernard Frigard</name></author><author><name sortKey="Destee, Alain" sort="Destee, Alain" uniqKey="Destee A" first="Alain" last="Destée">Alain Destée</name></author><author><name sortKey="Chartier Harlin, Marie Christine" sort="Chartier Harlin, Marie Christine" uniqKey="Chartier Harlin M" first="Marie-Christine" last="Chartier-Harlin">Marie-Christine Chartier-Harlin</name></author></analytic><series><title level="j">Neurobiology of aging</title><idno type="eISSN">1558-1497</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell Adhesion Molecules, Neuronal (genetics)</term><term>Female</term><term>Gene Expression Profiling (methods)</term><term>Humans</term><term>Leukocytes, Mononuclear (metabolism)</term><term>Male</term><term>Middle Aged</term><term>Mutation (genetics)</term><term>Oligonucleotide Array Sequence Analysis (methods)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Principal Component Analysis</term><term>Signal Transduction (genetics)</term><term>Statistics as Topic</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cell Adhesion Molecules, Neuronal</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Parkinson Disease</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Leukocytes, Mononuclear</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Gene Expression Profiling</term><term>Oligonucleotide Array Sequence Analysis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Principal Component Analysis</term><term>Statistics as Topic</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To gain insight into systemic molecular events associated with an age-related neurodegenerative disorder, we compared gene expression patterns in peripheral blood mononuclear cells (PBMCs) sampled from elderly, healthy controls and from Parkinson's disease (PD) patients carrying the most frequently found mutation of the LRRK2 gene (G2019S). A transcriptomic approach enabled us to detect differentially expressed genes and revealed perturbations of pathways known to be involved in PD-related neurodegeneration: the ubiquitin-proteasome system, the mitochondrial oxidation system, inflammation, axonal guidance, calcium signalling and apoptosis. Moreover, alterations of the MAP kinase pathway, the actin cytoskeleton, the ephrin receptor system and vesicular transport - all recently associated with the LRRK2 G2019S mutation pathogenesis - were noted. Furthermore, we acquired new evidences of dysregulation in leukocyte extravasation signalling and immune system pathways in PD. These data show that the G2019S mutation affects the entire body and highlight some of the molecular events observed in the brain. This PBMC transcriptomic approach could be used to better understand neurodegeneration in PD and decipher new pathogenetic mechanisms, even at early stages of the disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20096956</PMID><DateCreated><Year>2011</Year><Month>08</Month><Day>15</Day></DateCreated><DateCompleted><Year>2011</Year><Month>12</Month><Day>15</Day></DateCompleted><DateRevised><Year>2011</Year><Month>08</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-1497</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>10</Issue><PubDate><Year>2011</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neurobiology of aging</Title><ISOAbbreviation>Neurobiol. Aging</ISOAbbreviation></Journal><ArticleTitle>Transcriptional profile of Parkinson blood mononuclear cells with LRRK2 mutation.</ArticleTitle><Pagination><MedlinePgn>1839-48</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurobiolaging.2009.10.016</ELocationID><Abstract><AbstractText>To gain insight into systemic molecular events associated with an age-related neurodegenerative disorder, we compared gene expression patterns in peripheral blood mononuclear cells (PBMCs) sampled from elderly, healthy controls and from Parkinson's disease (PD) patients carrying the most frequently found mutation of the LRRK2 gene (G2019S). A transcriptomic approach enabled us to detect differentially expressed genes and revealed perturbations of pathways known to be involved in PD-related neurodegeneration: the ubiquitin-proteasome system, the mitochondrial oxidation system, inflammation, axonal guidance, calcium signalling and apoptosis. Moreover, alterations of the MAP kinase pathway, the actin cytoskeleton, the ephrin receptor system and vesicular transport - all recently associated with the LRRK2 G2019S mutation pathogenesis - were noted. Furthermore, we acquired new evidences of dysregulation in leukocyte extravasation signalling and immune system pathways in PD. These data show that the G2019S mutation affects the entire body and highlight some of the molecular events observed in the brain. This PBMC transcriptomic approach could be used to better understand neurodegeneration in PD and decipher new pathogenetic mechanisms, even at early stages of the disease.</AbstractText><CopyrightInformation>Copyright © 2009 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mutez</LastName><ForeName>Eugénie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Univ Lille Nord de France, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Larvor</LastName><ForeName>Lydie</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Leprêtre</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Mouroux</LastName><ForeName>Vincent</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Hamalek</LastName><ForeName>Dorota</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Kerckaert</LastName><ForeName>Jean-Pierre</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Pérez-Tur</LastName><ForeName>Jordi</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Waucquier</LastName><ForeName>Nawal</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Vanbesien-Mailliot</LastName><ForeName>Christel</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Duflot</LastName><ForeName>Aurélie</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Devos</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Defebvre</LastName><ForeName>Luc</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Kreisler</LastName><ForeName>Alexandre</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Frigard</LastName><ForeName>Bernard</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Destée</LastName><ForeName>Alain</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Chartier-Harlin</LastName><ForeName>Marie-Christine</ForeName><Initials>MC</Initials></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>2010</Year><Month>01</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Aging</MedlineTA><NlmUniqueID>8100437</NlmUniqueID><ISSNLinking>0197-4580</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015816">Cell Adhesion Molecules, Neuronal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C113373">LRRN2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015816" MajorTopicYN="N">Cell Adhesion Molecules, Neuronal</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007963" MajorTopicYN="N">Leukocytes, Mononuclear</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D025341" MajorTopicYN="N">Principal Component Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013223" MajorTopicYN="N">Statistics as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>02</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2009</Year><Month>10</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>10</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>1</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>1</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>12</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20096956</ArticleId><ArticleId IdType="pii">S0197-4580(09)00357-1</ArticleId><ArticleId IdType="doi">10.1016/j.neurobiolaging.2009.10.016</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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