Is differential regulation of mitochondrial transcripts in Parkinson's disease related to apoptosis?
Identifieur interne : 001395 ( PubMed/Checkpoint ); précédent : 001394; suivant : 001396Is differential regulation of mitochondrial transcripts in Parkinson's disease related to apoptosis?
Auteurs : M. Ruberg [France] ; B. Brugg ; A. Prigent ; E. Hirsch ; A. Brice ; Yves Agid [France]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 1997.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Apoptosis, DNA, Complementary (genetics), Female, Gene Library, Humans, In Situ Hybridization, Male, Mitochondria (physiology), Parkinson Disease (genetics), Parkinson Disease (pathology), Substantia Nigra (physiopathology), Transcription, Genetic, Tumor Necrosis Factor-alpha (pharmacology).
- MESH :
- chemical , genetics : DNA, Complementary.
- genetics : Parkinson Disease.
- pathology : Parkinson Disease.
- chemical , pharmacology : Tumor Necrosis Factor-alpha.
- physiology : Mitochondria.
- physiopathology : Substantia Nigra.
- Aged, Aged, 80 and over, Apoptosis, Female, Gene Library, Humans, In Situ Hybridization, Male, Transcription, Genetic.
Abstract
A cDNA library of substantia nigra pars compacta from a patient with Parkinson's disease (PD) was differentially screened with probes of normal and parkinsonian substantia nigra enriched in neuronal transcripts. Fifty-eight clones were isolated; 39 were subunits of mitochondrial respiratory complexes I and IV. Parallel screening of a cDNA library derived from normal substantia nigra confirmed differential representation of the transcripts in the substantia nigra pars compacta. In situ hybridization in postmortem brain from parkinsonian and control subjects, with representative complex I and complex IV probes, showed increased labeling, at the cellular level, of the complex I subunit ND1 in neurons of the lateral substantia nigra, where cell death is greatest in PD, but decreased labeling in the medial substantia nigra where fewer cells die. Expression of a complex IV subunit, COXI, increased, however, in both parts of the structure. Increased expression of ND1 and COXI was also observed in nerve growth factor-differentiated PC12 cells undergoing apoptosis induced by tumor necrosis factor-alpha, suggesting that the differential regulation of certain mitochondrial mRNAs may be associated with this form of cell death. This in vitro model of apoptosis is potentially relevant to the death of dopaminergic neurons in PD, because these cells express the tumor necrosis factor-alpha receptor, and neighboring microglial cells in patients synthesize the cytokine.
PubMed: 9109538
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Hirsch</name></author><author><name sortKey="Brice, A" sort="Brice, A" uniqKey="Brice A" first="A" last="Brice">A. Brice</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9109538</idno><idno type="pmid">9109538</idno><idno type="wicri:Area/PubMed/Corpus">001533</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001533</idno><idno type="wicri:Area/PubMed/Curation">001492</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001492</idno><idno type="wicri:Area/PubMed/Checkpoint">001492</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001492</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Is differential regulation of mitochondrial transcripts in Parkinson's disease related to apoptosis?</title><author><name sortKey="Ruberg, M" sort="Ruberg, M" uniqKey="Ruberg M" first="M" last="Ruberg">M. Ruberg</name><affiliation wicri:level="3"><nlm:affiliation>INSERM U289, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U289, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Brugg, B" sort="Brugg, B" uniqKey="Brugg B" first="B" last="Brugg">B. Brugg</name></author><author><name sortKey="Prigent, A" sort="Prigent, A" uniqKey="Prigent A" first="A" last="Prigent">A. Prigent</name></author><author><name sortKey="Hirsch, E" sort="Hirsch, E" uniqKey="Hirsch E" first="E" last="Hirsch">E. Hirsch</name></author><author><name sortKey="Brice, A" sort="Brice, A" uniqKey="Brice A" first="A" last="Brice">A. Brice</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="ISSN">0022-3042</idno><imprint><date when="1997" type="published">1997</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</term><term>DNA, Complementary (genetics)</term><term>Female</term><term>Gene Library</term><term>Humans</term><term>In Situ Hybridization</term><term>Male</term><term>Mitochondria (physiology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Substantia Nigra (physiopathology)</term><term>Transcription, Genetic</term><term>Tumor Necrosis Factor-alpha (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Complementary</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Apoptosis</term><term>Female</term><term>Gene Library</term><term>Humans</term><term>In Situ Hybridization</term><term>Male</term><term>Transcription, Genetic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A cDNA library of substantia nigra pars compacta from a patient with Parkinson's disease (PD) was differentially screened with probes of normal and parkinsonian substantia nigra enriched in neuronal transcripts. Fifty-eight clones were isolated; 39 were subunits of mitochondrial respiratory complexes I and IV. Parallel screening of a cDNA library derived from normal substantia nigra confirmed differential representation of the transcripts in the substantia nigra pars compacta. In situ hybridization in postmortem brain from parkinsonian and control subjects, with representative complex I and complex IV probes, showed increased labeling, at the cellular level, of the complex I subunit ND1 in neurons of the lateral substantia nigra, where cell death is greatest in PD, but decreased labeling in the medial substantia nigra where fewer cells die. Expression of a complex IV subunit, COXI, increased, however, in both parts of the structure. Increased expression of ND1 and COXI was also observed in nerve growth factor-differentiated PC12 cells undergoing apoptosis induced by tumor necrosis factor-alpha, suggesting that the differential regulation of certain mitochondrial mRNAs may be associated with this form of cell death. This in vitro model of apoptosis is potentially relevant to the death of dopaminergic neurons in PD, because these cells express the tumor necrosis factor-alpha receptor, and neighboring microglial cells in patients synthesize the cytokine.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9109538</PMID><DateCreated><Year>1997</Year><Month>05</Month><Day>15</Day></DateCreated><DateCompleted><Year>1997</Year><Month>05</Month><Day>15</Day></DateCompleted><DateRevised><Year>2004</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3042</ISSN><JournalIssue CitedMedium="Print"><Volume>68</Volume><Issue>5</Issue><PubDate><Year>1997</Year><Month>May</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Is differential regulation of mitochondrial transcripts in Parkinson's disease related to apoptosis?</ArticleTitle><Pagination><MedlinePgn>2098-110</MedlinePgn></Pagination><Abstract><AbstractText>A cDNA library of substantia nigra pars compacta from a patient with Parkinson's disease (PD) was differentially screened with probes of normal and parkinsonian substantia nigra enriched in neuronal transcripts. Fifty-eight clones were isolated; 39 were subunits of mitochondrial respiratory complexes I and IV. Parallel screening of a cDNA library derived from normal substantia nigra confirmed differential representation of the transcripts in the substantia nigra pars compacta. In situ hybridization in postmortem brain from parkinsonian and control subjects, with representative complex I and complex IV probes, showed increased labeling, at the cellular level, of the complex I subunit ND1 in neurons of the lateral substantia nigra, where cell death is greatest in PD, but decreased labeling in the medial substantia nigra where fewer cells die. Expression of a complex IV subunit, COXI, increased, however, in both parts of the structure. Increased expression of ND1 and COXI was also observed in nerve growth factor-differentiated PC12 cells undergoing apoptosis induced by tumor necrosis factor-alpha, suggesting that the differential regulation of certain mitochondrial mRNAs may be associated with this form of cell death. This in vitro model of apoptosis is potentially relevant to the death of dopaminergic neurons in PD, because these cells express the tumor necrosis factor-alpha receptor, and neighboring microglial cells in patients synthesize the cytokine.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ruberg</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>INSERM U289, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brugg</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Prigent</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Brice</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018076">DNA, Complementary</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</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="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018076" MajorTopicYN="N">DNA, Complementary</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015723" MajorTopicYN="N">Gene Library</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017403" MajorTopicYN="N">In Situ Hybridization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</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="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>5</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9109538</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><noCountry><name sortKey="Brice, A" sort="Brice, A" uniqKey="Brice A" first="A" last="Brice">A. Brice</name><name sortKey="Brugg, B" sort="Brugg, B" uniqKey="Brugg B" first="B" last="Brugg">B. Brugg</name><name sortKey="Hirsch, E" sort="Hirsch, E" uniqKey="Hirsch E" first="E" last="Hirsch">E. Hirsch</name><name sortKey="Prigent, A" sort="Prigent, A" uniqKey="Prigent A" first="A" last="Prigent">A. Prigent</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Ruberg, M" sort="Ruberg, M" uniqKey="Ruberg M" first="M" last="Ruberg">M. Ruberg</name></region><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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