Calpastatin immunoreactivity in the monkey and human brain of control subjects and patients with Parkinson's disease
Identifieur interne : 000404 ( Istex/Corpus ); précédent : 000403; suivant : 000405Calpastatin immunoreactivity in the monkey and human brain of control subjects and patients with Parkinson's disease
Auteurs : Annick Mouatt-Prigent ; Jan-Olof Karlsson ; Jerome Yelnik ; Yves Agid ; Etienne C. HirschSource :
- Journal of Comparative Neurology [ 0021-9967 ] ; 2000-04-03.
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Abstract
Parkinson's disease is characterized by a selective loss of dopaminergic neurons in the nigrostriatal pathway. However, not all dopaminergic neurons degenerate in this disease, and calcium has been suspected of playing a role in this differential vulnerability. An overexpression of the calcium‐dependent protease calpain II has recently been reported in the parkinsonian substantia nigra, suggesting that a rise in intracellular calcium concentrations may be involved in the mechanism leading to cell death. The proteasic activity of calpain is regulated by an endogenous inhibitory protein called calpastatin. Because little is known about the distribution of calpastatin in the primate brain, we first analyzed immunohistochemically the calpastatin expression in normal human and monkey brain. A ubiquitous distribution of calpastatin immunostaining was observed in both cases, but its expression was variable from one region to another. In the basal ganglia, staining was intense in the striatum, in the pallidal complex, and in some nuclei of the thalamus. The cerebellum was stained intensely, particularly in the granular and Purkinje cell layers. A dense, heterogeneous staining was observed in the hippocampal formation, mostly in the pyramidal and granular layers. The distribution of staining was similar in the different cerebral cortices studied, and it was most intense in layer V. In the brainstem, staining was particularly prominent in the substantia nigra pars reticulata and compacta, the central gray substance, the superior colliculus, and the cuneiform nucleus, and staining was moderate in the tegmenti pedonculopontinus nucleus and the griseum pontis. In the second part of the study, the authors compared calpastatin expression in the mesencephalon between patients with Parkinson's disease and control subjects. Sequential double staining revealed that some dopaminergic neurons coexpress calpastatin, the proportion of double‐stained neurons ranging between 52% and 76% among the different dopaminergic cell groups. Quantitative analysis of the number of calpastatin‐stained neurons evidenced a loss of both calpastatin‐positive and calpastatin‐negative neurons in the substantia nigra of patients with Parkinson's disease. These data suggest that calpain II overexpression in Parkinson's disease is not compensated for by a concomitant increase in calpastatin expression. J. Comp. Neurol. 419:175–192, 2000. © 2000 Wiley‐Liss, Inc.
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DOI: 10.1002/(SICI)1096-9861(20000403)419:2<175::AID-CNE3>3.0.CO;2-2
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However, not all dopaminergic neurons degenerate in this disease, and calcium has been suspected of playing a role in this differential vulnerability. An overexpression of the calcium‐dependent protease calpain II has recently been reported in the parkinsonian substantia nigra, suggesting that a rise in intracellular calcium concentrations may be involved in the mechanism leading to cell death. The proteasic activity of calpain is regulated by an endogenous inhibitory protein called calpastatin. Because little is known about the distribution of calpastatin in the primate brain, we first analyzed immunohistochemically the calpastatin expression in normal human and monkey brain. A ubiquitous distribution of calpastatin immunostaining was observed in both cases, but its expression was variable from one region to another. In the basal ganglia, staining was intense in the striatum, in the pallidal complex, and in some nuclei of the thalamus. The cerebellum was stained intensely, particularly in the granular and Purkinje cell layers. A dense, heterogeneous staining was observed in the hippocampal formation, mostly in the pyramidal and granular layers. The distribution of staining was similar in the different cerebral cortices studied, and it was most intense in layer V. In the brainstem, staining was particularly prominent in the substantia nigra pars reticulata and compacta, the central gray substance, the superior colliculus, and the cuneiform nucleus, and staining was moderate in the tegmenti pedonculopontinus nucleus and the griseum pontis. In the second part of the study, the authors compared calpastatin expression in the mesencephalon between patients with Parkinson's disease and control subjects. Sequential double staining revealed that some dopaminergic neurons coexpress calpastatin, the proportion of double‐stained neurons ranging between 52% and 76% among the different dopaminergic cell groups. Quantitative analysis of the number of calpastatin‐stained neurons evidenced a loss of both calpastatin‐positive and calpastatin‐negative neurons in the substantia nigra of patients with Parkinson's disease. These data suggest that calpain II overexpression in Parkinson's disease is not compensated for by a concomitant increase in calpastatin expression. J. Comp. Neurol. 419:175–192, 2000. © 2000 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Annick Mouatt‐Prigent</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Jan‐Olof Karlsson</name><affiliations><json:string>Institute of Anatomy and Cell Biology, Göteborg University, SE 405 30 Göteborg, Sweden</json:string></affiliations></json:item><json:item><name>Jerome Yelnik</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Yves Agid</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Etienne C. 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The cerebellum was stained intensely, particularly in the granular and Purkinje cell layers. A dense, heterogeneous staining was observed in the hippocampal formation, mostly in the pyramidal and granular layers. The distribution of staining was similar in the different cerebral cortices studied, and it was most intense in layer V. In the brainstem, staining was particularly prominent in the substantia nigra pars reticulata and compacta, the central gray substance, the superior colliculus, and the cuneiform nucleus, and staining was moderate in the tegmenti pedonculopontinus nucleus and the griseum pontis. In the second part of the study, the authors compared calpastatin expression in the mesencephalon between patients with Parkinson's disease and control subjects. Sequential double staining revealed that some dopaminergic neurons coexpress calpastatin, the proportion of double‐stained neurons ranging between 52% and 76% among the different dopaminergic cell groups. Quantitative analysis of the number of calpastatin‐stained neurons evidenced a loss of both calpastatin‐positive and calpastatin‐negative neurons in the substantia nigra of patients with Parkinson's disease. These data suggest that calpain II overexpression in Parkinson's disease is not compensated for by a concomitant increase in calpastatin expression. J. Comp. 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The cerebellum was stained intensely, particularly in the granular and Purkinje cell layers. A dense, heterogeneous staining was observed in the hippocampal formation, mostly in the pyramidal and granular layers. The distribution of staining was similar in the different cerebral cortices studied, and it was most intense in layer V. In the brainstem, staining was particularly prominent in the substantia nigra pars reticulata and compacta, the central gray substance, the superior colliculus, and the cuneiform nucleus, and staining was moderate in the tegmenti pedonculopontinus nucleus and the griseum pontis. In the second part of the study, the authors compared calpastatin expression in the mesencephalon between patients with Parkinson's disease and control subjects. Sequential double staining revealed that some dopaminergic neurons coexpress calpastatin, the proportion of double‐stained neurons ranging between 52% and 76% among the different dopaminergic cell groups. Quantitative analysis of the number of calpastatin‐stained neurons evidenced a loss of both calpastatin‐positive and calpastatin‐negative neurons in the substantia nigra of patients with Parkinson's disease. These data suggest that calpain II overexpression in Parkinson's disease is not compensated for by a concomitant increase in calpastatin expression. J. Comp. Neurol. 419:175–192, 2000. © 2000 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>calcium</term></item><item><term>cell death</term></item><item><term>calpain</term></item><item><term>dopamine</term></item><item><term>substantia nigra</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-07-01">Received</change><change when="1999-11-16">Registration</change><change when="2000-04-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/22ACE0AECD36C7164F473C65C68B5C782D6A48BF/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1096-9861</doi><issn type="print">0021-9967</issn><issn type="electronic">1096-9861</issn><idGroup><id type="product" value="CNE"></id></idGroup><titleGroup><title type="main" xml:lang="en">Journal of Comparative Neurology</title><title type="short">J. 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Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/(SICI)1096-9861(20000403)419:2<>1.0.CO;2-X</doi><numberingGroup><numbering type="journalVolume" number="419">419</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="2000-04-03">3 April 2000</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley" registered="yes">10.1002/(SICI)1096-9861(20000403)419:2<175::AID-CNE3>3.0.CO;2-2</doi><idGroup><id type="unit" value="CNE3"></id></idGroup><countGroup><count type="pageTotal" number="18"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">ARTICLES</title></titleGroup><copyright ownership="publisher">Copyright © 2000 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="1998-07-01"></event><event type="manuscriptRevised" date="1999-11-12"></event><event type="manuscriptAccepted" date="1999-11-16"></event><event type="firstOnline" date="2000-03-17"></event><event type="publishedOnlineFinalForm" date="2000-03-17"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-01"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">175</numbering><numbering type="pageLast">192</numbering></numberingGroup><correspondenceTo>INSERM U289, Hôpital de la Salpêtrière, 47 Boulevard de l'hôpital, 75013 Paris, France</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CNE.CNE3.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="14"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="7891"></count></countGroup><titleGroup><title type="main" xml:lang="en">Calpastatin immunoreactivity in the monkey and human brain of control subjects and patients with Parkinson's disease</title><title type="short" xml:lang="en">CALPASTATIN IN PRIMATE BRAIN</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Annick</givenNames><familyName>Mouatt‐Prigent</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jan‐Olof</givenNames><familyName>Karlsson</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jerome</givenNames><familyName>Yelnik</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yves</givenNames><familyName>Agid</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Etienne C.</givenNames><familyName>Hirsch</familyName></personName><contactDetails><email>hirsch@ccr.jussieu.fr</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="SE" type="organization"><unparsedAffiliation>Institute of Anatomy and Cell Biology, Göteborg University, SE 405 30 Göteborg, Sweden</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">calcium</keyword><keyword xml:id="kwd2">cell death</keyword><keyword xml:id="kwd3">calpain</keyword><keyword xml:id="kwd4">dopamine</keyword><keyword xml:id="kwd5">substantia nigra</keyword></keywordGroup><fundingInfo><fundingAgency>Institut National de la Santé et de la Recherche Médicale</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson's Disease Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson's disease is characterized by a selective loss of dopaminergic neurons in the nigrostriatal pathway. However, not all dopaminergic neurons degenerate in this disease, and calcium has been suspected of playing a role in this differential vulnerability. An overexpression of the calcium‐dependent protease calpain II has recently been reported in the parkinsonian substantia nigra, suggesting that a rise in intracellular calcium concentrations may be involved in the mechanism leading to cell death. The proteasic activity of calpain is regulated by an endogenous inhibitory protein called calpastatin. Because little is known about the distribution of calpastatin in the primate brain, we first analyzed immunohistochemically the calpastatin expression in normal human and monkey brain. A ubiquitous distribution of calpastatin immunostaining was observed in both cases, but its expression was variable from one region to another. In the basal ganglia, staining was intense in the striatum, in the pallidal complex, and in some nuclei of the thalamus. The cerebellum was stained intensely, particularly in the granular and Purkinje cell layers. A dense, heterogeneous staining was observed in the hippocampal formation, mostly in the pyramidal and granular layers. The distribution of staining was similar in the different cerebral cortices studied, and it was most intense in layer V. In the brainstem, staining was particularly prominent in the substantia nigra pars reticulata and compacta, the central gray substance, the superior colliculus, and the cuneiform nucleus, and staining was moderate in the tegmenti pedonculopontinus nucleus and the griseum pontis. In the second part of the study, the authors compared calpastatin expression in the mesencephalon between patients with Parkinson's disease and control subjects. Sequential double staining revealed that some dopaminergic neurons coexpress calpastatin, the proportion of double‐stained neurons ranging between 52% and 76% among the different dopaminergic cell groups. Quantitative analysis of the number of calpastatin‐stained neurons evidenced a loss of both calpastatin‐positive and calpastatin‐negative neurons in the substantia nigra of patients with Parkinson's disease. These data suggest that calpain II overexpression in Parkinson's disease is not compensated for by a concomitant increase in calpastatin expression. J. Comp. Neurol. 419:175–192, 2000. © 2000 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Calpastatin immunoreactivity in the monkey and human brain of control subjects and patients with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CALPASTATIN IN PRIMATE BRAIN</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Calpastatin immunoreactivity in the monkey and human brain of control subjects and patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Annick</namePart><namePart type="family">Mouatt‐Prigent</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan‐Olof</namePart><namePart type="family">Karlsson</namePart><affiliation>Institute of Anatomy and Cell Biology, Göteborg University, SE 405 30 Göteborg, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jerome</namePart><namePart type="family">Yelnik</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etienne C.</namePart><namePart type="family">Hirsch</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><affiliation>INSERM U289, Hôpital de la Salpêtrière, 47 Boulevard de l'hôpital, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2000-04-03</dateIssued><dateCaptured encoding="w3cdtf">1998-07-01</dateCaptured><dateValid encoding="w3cdtf">1999-11-16</dateValid><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">14</extent><extent unit="tables">2</extent><extent unit="references">33</extent><extent unit="words">7891</extent></physicalDescription><abstract lang="en">Parkinson's disease is characterized by a selective loss of dopaminergic neurons in the nigrostriatal pathway. However, not all dopaminergic neurons degenerate in this disease, and calcium has been suspected of playing a role in this differential vulnerability. An overexpression of the calcium‐dependent protease calpain II has recently been reported in the parkinsonian substantia nigra, suggesting that a rise in intracellular calcium concentrations may be involved in the mechanism leading to cell death. The proteasic activity of calpain is regulated by an endogenous inhibitory protein called calpastatin. Because little is known about the distribution of calpastatin in the primate brain, we first analyzed immunohistochemically the calpastatin expression in normal human and monkey brain. A ubiquitous distribution of calpastatin immunostaining was observed in both cases, but its expression was variable from one region to another. In the basal ganglia, staining was intense in the striatum, in the pallidal complex, and in some nuclei of the thalamus. The cerebellum was stained intensely, particularly in the granular and Purkinje cell layers. A dense, heterogeneous staining was observed in the hippocampal formation, mostly in the pyramidal and granular layers. The distribution of staining was similar in the different cerebral cortices studied, and it was most intense in layer V. In the brainstem, staining was particularly prominent in the substantia nigra pars reticulata and compacta, the central gray substance, the superior colliculus, and the cuneiform nucleus, and staining was moderate in the tegmenti pedonculopontinus nucleus and the griseum pontis. In the second part of the study, the authors compared calpastatin expression in the mesencephalon between patients with Parkinson's disease and control subjects. Sequential double staining revealed that some dopaminergic neurons coexpress calpastatin, the proportion of double‐stained neurons ranging between 52% and 76% among the different dopaminergic cell groups. Quantitative analysis of the number of calpastatin‐stained neurons evidenced a loss of both calpastatin‐positive and calpastatin‐negative neurons in the substantia nigra of patients with Parkinson's disease. These data suggest that calpain II overexpression in Parkinson's disease is not compensated for by a concomitant increase in calpastatin expression. J. Comp. Neurol. 419:175–192, 2000. © 2000 Wiley‐Liss, Inc.</abstract><note type="funding">Institut National de la Santé et de la Recherche Médicale</note><note type="funding">National Parkinson's Disease Foundation</note><subject lang="en"><genre>keywords</genre><topic>calcium</topic><topic>cell death</topic><topic>calpain</topic><topic>dopamine</topic><topic>substantia nigra</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Comparative Neurology</title></titleInfo><titleInfo type="abbreviated"><title>J. Comp. 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