Tyrosine hydroxylase protein and messenger RNA in the dopaminergic nigral neurons of patients with Parkinson's disease.
Identifieur interne : 001722 ( PubMed/Corpus ); précédent : 001721; suivant : 001723Tyrosine hydroxylase protein and messenger RNA in the dopaminergic nigral neurons of patients with Parkinson's disease.
Auteurs : A. Kastner ; E C Hirsch ; Y. Agid ; F. Javoy-AgidSource :
- Brain research [ 0006-8993 ] ; 1993.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Autoradiography, Dopamine (metabolism), Female, Humans, Immunohistochemistry, In Situ Hybridization, Male, Middle Aged, Neurons (metabolism), Parkinson Disease (metabolism), Parkinson Disease (pathology), RNA, Messenger (metabolism), Substantia Nigra (metabolism), Substantia Nigra (pathology), Tyrosine 3-Monooxygenase (genetics), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , genetics : Tyrosine 3-Monooxygenase.
- chemical , metabolism : Dopamine, RNA, Messenger, Tyrosine 3-Monooxygenase.
- metabolism : Neurons, Parkinson Disease, Substantia Nigra.
- pathology : Parkinson Disease, Substantia Nigra.
- Aged, Aged, 80 and over, Autoradiography, Female, Humans, Immunohistochemistry, In Situ Hybridization, Male, Middle Aged.
Abstract
To analyze the roles of transcriptional and post-transcriptional regulatory mechanisms of tyrosine hydroxylase (TH) gene expression during dopaminergic denervation in Parkinson's disease (PD), the cellular content of TH messenger RNA (mRNA) and TH protein in the substantia nigra were compared in control subjects and patients with PD. The average amounts of TH mRNA as well as those of TH protein per neuron were variable among controls but correlated to each other. In PD patients, both TH mRNA and TH protein content in nigral neurons were reduced relative to controls, however, the ratio between TH protein and TH mRNA levels was unaffected. The data suggest that, in PD: (1) TH protein content is decreased in the surviving nigral dopaminergic neurons, most likely as a result of a lowered TH mRNA cellular content. Thus the surviving neurons at end stages of the disease may be in a premorbid state. (2) The TH mRNA translation rate is not modified to compensate for dopamine deficiency.
PubMed: 8098254
Links to Exploration step
pubmed:8098254Le document en format XML
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Javoy-Agid</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8098254</idno><idno type="pmid">8098254</idno><idno type="wicri:Area/PubMed/Corpus">001722</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001722</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Tyrosine hydroxylase protein and messenger RNA in the dopaminergic nigral neurons of patients with Parkinson's disease.</title><author><name sortKey="Kastner, A" sort="Kastner, A" uniqKey="Kastner A" first="A" last="Kastner">A. Kastner</name><affiliation><nlm:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Javoy Agid, F" sort="Javoy Agid, F" uniqKey="Javoy Agid F" first="F" last="Javoy-Agid">F. Javoy-Agid</name></author></analytic><series><title level="j">Brain research</title><idno type="ISSN">0006-8993</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Autoradiography</term><term>Dopamine (metabolism)</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>In Situ Hybridization</term><term>Male</term><term>Middle Aged</term><term>Neurons (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>RNA, Messenger (metabolism)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Tyrosine 3-Monooxygenase (genetics)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>RNA, Messenger</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Autoradiography</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>In Situ Hybridization</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To analyze the roles of transcriptional and post-transcriptional regulatory mechanisms of tyrosine hydroxylase (TH) gene expression during dopaminergic denervation in Parkinson's disease (PD), the cellular content of TH messenger RNA (mRNA) and TH protein in the substantia nigra were compared in control subjects and patients with PD. The average amounts of TH mRNA as well as those of TH protein per neuron were variable among controls but correlated to each other. In PD patients, both TH mRNA and TH protein content in nigral neurons were reduced relative to controls, however, the ratio between TH protein and TH mRNA levels was unaffected. The data suggest that, in PD: (1) TH protein content is decreased in the surviving nigral dopaminergic neurons, most likely as a result of a lowered TH mRNA cellular content. Thus the surviving neurons at end stages of the disease may be in a premorbid state. (2) The TH mRNA translation rate is not modified to compensate for dopamine deficiency.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8098254</PMID><DateCreated><Year>1993</Year><Month>06</Month><Day>14</Day></DateCreated><DateCompleted><Year>1993</Year><Month>06</Month><Day>14</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8993</ISSN><JournalIssue CitedMedium="Print"><Volume>606</Volume><Issue>2</Issue><PubDate><Year>1993</Year><Month>Mar</Month><Day>26</Day></PubDate></JournalIssue><Title>Brain research</Title><ISOAbbreviation>Brain Res.</ISOAbbreviation></Journal><ArticleTitle>Tyrosine hydroxylase protein and messenger RNA in the dopaminergic nigral neurons of patients with Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>341-5</MedlinePgn></Pagination><Abstract><AbstractText>To analyze the roles of transcriptional and post-transcriptional regulatory mechanisms of tyrosine hydroxylase (TH) gene expression during dopaminergic denervation in Parkinson's disease (PD), the cellular content of TH messenger RNA (mRNA) and TH protein in the substantia nigra were compared in control subjects and patients with PD. The average amounts of TH mRNA as well as those of TH protein per neuron were variable among controls but correlated to each other. In PD patients, both TH mRNA and TH protein content in nigral neurons were reduced relative to controls, however, the ratio between TH protein and TH mRNA levels was unaffected. The data suggest that, in PD: (1) TH protein content is decreased in the surviving nigral dopaminergic neurons, most likely as a result of a lowered TH mRNA cellular content. Thus the surviving neurons at end stages of the disease may be in a premorbid state. (2) The TH mRNA translation rate is not modified to compensate for dopamine deficiency.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kastner</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Javoy-Agid</LastName><ForeName>F</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Brain Res</MedlineTA><NlmUniqueID>0045503</NlmUniqueID><ISSNLinking>0006-8993</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</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="D001345" MajorTopicYN="N">Autoradiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</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="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1993</Year><Month>3</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>3</Month><Day>26</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>3</Month><Day>26</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8098254</ArticleId><ArticleId IdType="pii">0006-8993(93)91005-D</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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