Increased expression and redistribution of the antiapoptotic molecule Bcl-xL in Parkinson's disease.
Identifieur interne : 001188 ( PubMed/Corpus ); précédent : 001187; suivant : 001189Increased expression and redistribution of the antiapoptotic molecule Bcl-xL in Parkinson's disease.
Auteurs : Andreas Hartmann ; Annick Mouatt-Prigent ; Miquel Vila ; Nacer Abbas ; Céline Perier ; Baptiste A. Faucheux ; Sheela Vyas ; Etienne C. HirschSource :
- Neurobiology of disease [ 0969-9961 ] ; 2002.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Apoptosis (physiology), Dihydroxyphenylalanine (physiology), Humans, Melanins (metabolism), Mesencephalon (metabolism), Mesencephalon (ultrastructure), Neurons (metabolism), Neurons (physiology), Neurons (ultrastructure), Organ Specificity, Parkinson Disease (metabolism), Parkinson Disease (pathology), Proto-Oncogene Proteins c-bcl-2 (biosynthesis), Proto-Oncogene Proteins c-bcl-2 (metabolism), Proto-Oncogene Proteins c-bcl-2 (ultrastructure), RNA, Messenger (biosynthesis), bcl-X Protein.
- MESH :
- chemical , biosynthesis : Proto-Oncogene Proteins c-bcl-2, RNA, Messenger.
- chemical , metabolism : Melanins, Proto-Oncogene Proteins c-bcl-2.
- chemical , physiology : Dihydroxyphenylalanine.
- metabolism : Mesencephalon, Neurons, Parkinson Disease.
- pathology : Parkinson Disease.
- physiology : Apoptosis, Neurons.
- ultrastructure : Mesencephalon, Neurons, Proto-Oncogene Proteins c-bcl-2.
- Aged, Aged, 80 and over, Humans, Organ Specificity, bcl-X Protein.
Abstract
In the present study, we tried to clarify the potentially protective role of Bcl-x(L), an anti-apoptotic member of the Bcl-2 family of proteins, in Parkinson's disease (PD). Using in situ hybridization on human postmortem mesencephalon sections, we show that in PD patients Bcl-x(L) mRNA expression per dopaminergic neuron was almost double that of controls. We also show that, ultrastructurally, this effect may be mediated by a redistribution of Bcl-x(L) from the cytosol to the outer mitochondrial membrane.
PubMed: 12079401
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pubmed:12079401Le document en format XML
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Faucheux</name></author><author><name sortKey="Vyas, Sheela" sort="Vyas, Sheela" uniqKey="Vyas S" first="Sheela" last="Vyas">Sheela Vyas</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. 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Faucheux</name></author><author><name sortKey="Vyas, Sheela" sort="Vyas, Sheela" uniqKey="Vyas S" first="Sheela" last="Vyas">Sheela Vyas</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="ISSN">0969-9961</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Apoptosis (physiology)</term><term>Dihydroxyphenylalanine (physiology)</term><term>Humans</term><term>Melanins (metabolism)</term><term>Mesencephalon (metabolism)</term><term>Mesencephalon (ultrastructure)</term><term>Neurons (metabolism)</term><term>Neurons (physiology)</term><term>Neurons (ultrastructure)</term><term>Organ Specificity</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Proto-Oncogene Proteins c-bcl-2 (biosynthesis)</term><term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term><term>Proto-Oncogene Proteins c-bcl-2 (ultrastructure)</term><term>RNA, Messenger (biosynthesis)</term><term>bcl-X Protein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Proto-Oncogene Proteins c-bcl-2</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Melanins</term><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dihydroxyphenylalanine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mesencephalon</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Mesencephalon</term><term>Neurons</term><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Humans</term><term>Organ Specificity</term><term>bcl-X Protein</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the present study, we tried to clarify the potentially protective role of Bcl-x(L), an anti-apoptotic member of the Bcl-2 family of proteins, in Parkinson's disease (PD). Using in situ hybridization on human postmortem mesencephalon sections, we show that in PD patients Bcl-x(L) mRNA expression per dopaminergic neuron was almost double that of controls. We also show that, ultrastructurally, this effect may be mediated by a redistribution of Bcl-x(L) from the cytosol to the outer mitochondrial membrane.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12079401</PMID><DateCreated><Year>2002</Year><Month>06</Month><Day>24</Day></DateCreated><DateCompleted><Year>2002</Year><Month>08</Month><Day>21</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0969-9961</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><Issue>1</Issue><PubDate><Year>2002</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>Increased expression and redistribution of the antiapoptotic molecule Bcl-xL in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>28-32</MedlinePgn></Pagination><Abstract><AbstractText>In the present study, we tried to clarify the potentially protective role of Bcl-x(L), an anti-apoptotic member of the Bcl-2 family of proteins, in Parkinson's disease (PD). Using in situ hybridization on human postmortem mesencephalon sections, we show that in PD patients Bcl-x(L) mRNA expression per dopaminergic neuron was almost double that of controls. We also show that, ultrastructurally, this effect may be mediated by a redistribution of Bcl-x(L) from the cytosol to the outer mitochondrial membrane.</AbstractText><CopyrightInformation>2002 Elsevier Science (USA).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hartmann</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mouatt-Prigent</LastName><ForeName>Annick</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Vila</LastName><ForeName>Miquel</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Abbas</LastName><ForeName>Nacer</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Perier</LastName><ForeName>Céline</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Faucheux</LastName><ForeName>Baptiste A</ForeName><Initials>BA</Initials></Author><Author ValidYN="Y"><LastName>Vyas</LastName><ForeName>Sheela</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494811">BCL2L1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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