Increased M-calpain expression in the mesencephalon of patients with Parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?
Identifieur interne : 001571 ( PubMed/Corpus ); précédent : 001570; suivant : 001572Increased M-calpain expression in the mesencephalon of patients with Parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?
Auteurs : A. Mouatt-Prigent ; J O Karlsson ; Y. Agid ; E C HirschSource :
- Neuroscience [ 0306-4522 ] ; 1996.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Brain Diseases (metabolism), Brain Diseases (pathology), Calpain (metabolism), Cell Death, Corpus Striatum (pathology), Humans, Mesencephalon (metabolism), Mesencephalon (pathology), Middle Aged, Nerve Degeneration, Neurons (physiology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Reference Values, Staining and Labeling, Substantia Nigra (pathology), Supranuclear Palsy, Progressive (metabolism), Tyrosine 3-Monooxygenase (metabolism), Ubiquitins (metabolism).
- MESH :
- chemical , metabolism : Calpain, Tyrosine 3-Monooxygenase, Ubiquitins.
- metabolism : Brain Diseases, Mesencephalon, Parkinson Disease, Supranuclear Palsy, Progressive.
- pathology : Brain Diseases, Corpus Striatum, Mesencephalon, Parkinson Disease, Substantia Nigra.
- physiology : Neurons.
- Aged, Aged, 80 and over, Cell Death, Humans, Middle Aged, Nerve Degeneration, Reference Values, Staining and Labeling.
Abstract
Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures. These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.
PubMed: 8809817
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Agid</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8809817</idno><idno type="pmid">8809817</idno><idno type="wicri:Area/PubMed/Corpus">001571</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001571</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Increased M-calpain expression in the mesencephalon of patients with Parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?</title><author><name sortKey="Mouatt Prigent, A" sort="Mouatt Prigent, A" uniqKey="Mouatt Prigent A" first="A" last="Mouatt-Prigent">A. Mouatt-Prigent</name><affiliation><nlm:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Karlsson, J O" sort="Karlsson, J O" uniqKey="Karlsson J" first="J O" last="Karlsson">J O Karlsson</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></analytic><series><title level="j">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Brain Diseases (metabolism)</term><term>Brain Diseases (pathology)</term><term>Calpain (metabolism)</term><term>Cell Death</term><term>Corpus Striatum (pathology)</term><term>Humans</term><term>Mesencephalon (metabolism)</term><term>Mesencephalon (pathology)</term><term>Middle Aged</term><term>Nerve Degeneration</term><term>Neurons (physiology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Reference Values</term><term>Staining and Labeling</term><term>Substantia Nigra (pathology)</term><term>Supranuclear Palsy, Progressive (metabolism)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term><term>Ubiquitins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calpain</term><term>Tyrosine 3-Monooxygenase</term><term>Ubiquitins</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain Diseases</term><term>Mesencephalon</term><term>Parkinson Disease</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain Diseases</term><term>Corpus Striatum</term><term>Mesencephalon</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell Death</term><term>Humans</term><term>Middle Aged</term><term>Nerve Degeneration</term><term>Reference Values</term><term>Staining and Labeling</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures. These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8809817</PMID><DateCreated><Year>1997</Year><Month>02</Month><Day>19</Day></DateCreated><DateCompleted><Year>1997</Year><Month>02</Month><Day>19</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0306-4522</ISSN><JournalIssue CitedMedium="Print"><Volume>73</Volume><Issue>4</Issue><PubDate><Year>1996</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Neuroscience</Title><ISOAbbreviation>Neuroscience</ISOAbbreviation></Journal><ArticleTitle>Increased M-calpain expression in the mesencephalon of patients with Parkinson's disease but not in other neurodegenerative disorders involving the mesencephalon: a role in nerve cell death?</ArticleTitle><Pagination><MedlinePgn>979-87</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra and, to a lesser extent, the ventral tegmental area and catecholaminergic cell group A8. However, among these dopaminergic neurons, those expressing the calcium buffering protein calbindin are selectively preserved, suggesting that a rise in intracellular calcium concentrations may be involved in the cascade of events leading to nerve cell death in Parkinson's disease. We therefore analysed immunohistochemically the expression of the calcium-dependent protease calpain II (m-calpain) in the mesencephalon of patients with Parkinson's disease, progressive supranuclear palsy or striatonigral degeneration, where nigral dopaminergic neurons degenerate, and matched controls without nigral involvement. Calpain immunoreactivity was found in fibers and neuronal perikarya in the substantia nigra, the ventral tegmental area, catecholaminergic cell group A8 and the locus coeruleus. In patients with Parkinson's disease but not with the other neurodegenerative disorders, m-calpain immunoreactivity was detected in fibers with an abnormal morphology and in Lewy bodies. Sequential double staining revealed that most of these m-calpain-positive fibers and neuronal perikarya co-expressed tyrosine hydroxylase, indicating that most m-calpain neurons are catecholaminergic. Quantitative analysis of m-calpain staining in the substantia nigra and locus coeruleus revealed an increased density of fibers and neuronal perikarya in parkinsonian patients in both structures. These data suggest that increased calcium concentrations may be associated with nerve cell death in Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mouatt-Prigent</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karlsson</LastName><ForeName>J O</ForeName><Initials>JO</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neuroscience</MedlineTA><NlmUniqueID>7605074</NlmUniqueID><ISSNLinking>0306-4522</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014452">Ubiquitins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D002154">Calpain</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="D001927" MajorTopicYN="N">Brain Diseases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002154" MajorTopicYN="N">Calpain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008636" MajorTopicYN="N">Mesencephalon</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="Y">Nerve Degeneration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</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="D012016" MajorTopicYN="N">Reference Values</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013194" MajorTopicYN="N">Staining and Labeling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013494" MajorTopicYN="N">Supranuclear Palsy, Progressive</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014452" MajorTopicYN="N">Ubiquitins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>8</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>8</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>8</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8809817</ArticleId><ArticleId IdType="pii">0306-4522(96)00100-5</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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