Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases
Identifieur interne : 002549 ( Istex/Corpus ); précédent : 002548; suivant : 002550Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases
Auteurs : Douglas G. Walker ; Kazuhiro Terai ; Akinori Matsuo ; Thomas G. Beach ; Edith G. Mcgeer ; Patrick L. McgeerSource :
- Brain Research [ 0006-8993 ] ; 1998.
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Abstract
The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.
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DOI: 10.1016/S0006-8993(98)00132-2
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Walker</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>1Present address: Sun Health Research Institute, Sun City, AZ, USA.</mods:affiliation></affiliation></author><author><name sortKey="Terai, Kazuhiro" sort="Terai, Kazuhiro" uniqKey="Terai K" first="Kazuhiro" last="Terai">Kazuhiro Terai</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>2Present address: Yamanouchi Pharmaceutical Company, Japan.</mods:affiliation></affiliation></author><author><name sortKey="Matsuo, Akinori" sort="Matsuo, Akinori" uniqKey="Matsuo A" first="Akinori" last="Matsuo">Akinori Matsuo</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>3Present address: Department of Neurology, Kyoto University, Japan.</mods:affiliation></affiliation></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G" last="Beach">Thomas G. Beach</name><affiliation><mods:affiliation>Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>4Present address: Sun Health Research Institute, Sun City, AZ, USA.</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. 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Walker</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>1Present address: Sun Health Research Institute, Sun City, AZ, USA.</mods:affiliation></affiliation></author><author><name sortKey="Terai, Kazuhiro" sort="Terai, Kazuhiro" uniqKey="Terai K" first="Kazuhiro" last="Terai">Kazuhiro Terai</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>2Present address: Yamanouchi Pharmaceutical Company, Japan.</mods:affiliation></affiliation></author><author><name sortKey="Matsuo, Akinori" sort="Matsuo, Akinori" uniqKey="Matsuo A" first="Akinori" last="Matsuo">Akinori Matsuo</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>3Present address: Department of Neurology, Kyoto University, Japan.</mods:affiliation></affiliation></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G" last="Beach">Thomas G. Beach</name><affiliation><mods:affiliation>Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>4Present address: Sun Health Research Institute, Sun City, AZ, USA.</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada. Fax: +1-604-822-7086; E-mail: mcgeerpl@unixg.ubc.ca</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">794</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="181">181</biblScope><biblScope unit="page" to="187">187</biblScope></imprint><idno type="ISSN">0006-8993</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell death</term><term>Dopaminergic</term><term>Neurodegeneration</term><term>Neuron</term><term>Tyrosine kinase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Douglas G Walker</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</json:string><json:string>1Present address: Sun Health Research Institute, Sun City, AZ, USA.</json:string></affiliations></json:item><json:item><name>Kazuhiro Terai</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</json:string><json:string>2Present address: Yamanouchi Pharmaceutical Company, Japan.</json:string></affiliations></json:item><json:item><name>Akinori Matsuo</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</json:string><json:string>3Present address: Department of Neurology, Kyoto University, Japan.</json:string></affiliations></json:item><json:item><name>Thomas G Beach</name><affiliations><json:string>Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</json:string><json:string>4Present address: Sun Health Research Institute, Sun City, AZ, USA.</json:string></affiliations></json:item><json:item><name>Edith G McGeer</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</json:string></affiliations></json:item><json:item><name>Patrick L McGeer</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</json:string><json:string>Corresponding author. Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada. Fax: +1-604-822-7086; E-mail: mcgeerpl@unixg.ubc.ca</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dopaminergic</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cell death</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neurodegeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Tyrosine kinase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neuron</value></json:item></subject><articleId><json:string>14466</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.</abstract><qualityIndicators><score>6.285</score><pdfWordCount>4293</pdfWordCount><pdfCharCount>26642</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>595 x 738 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>166</abstractWordCount><abstractCharCount>1040</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases</title><pii><json:string>S0006-8993(98)00132-2</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Brain Research</title><language><json:string>unknown</json:string></language><publicationDate>1998</publicationDate><issn><json:string>0006-8993</json:string></issn><pii><json:string>S0006-8993(00)X0162-X</json:string></pii><volume>794</volume><issue>2</issue><pages><first>181</first><last>187</last></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1016/S0006-8993(98)00132-2</json:string></doi><id>2E7AC6F53C260874E27058A3EF0823895208CCBC</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/2E7AC6F53C260874E27058A3EF0823895208CCBC/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/2E7AC6F53C260874E27058A3EF0823895208CCBC/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/2E7AC6F53C260874E27058A3EF0823895208CCBC/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©1998 Elsevier Science B.V.</p></availability><date>1998</date></publicationStmt><notesStmt><note type="content">Section title: Research report</note><note type="content">Fig. 1: (A) Strong FGFR-1 immunoreactivity can be demonstrated in pigmented SN dopaminergic neurons in a tissue section from a young control case (YC2). Section was stained with the polyclonal antibody to FGFR-1. (B) Parallel section to that demonstrated in panel A. The antibody used was preabsorbed with an excess of the immunizing peptide before the tissue incubation stage. Notice that the immunoreactivity demonstrated in the SN DA neurons in panel A has been abolished. (C) Immunoblot analyses of membrane extract derived from the SN of a control case. Lane a) demonstrates two main bands, with molecular weights of approximately 130–140 kD. They appear to represent FGFR-1 with three Ig domains. Lane b) shows the results of a parallel section of membrane to that in lane a) except that the antibody had been preincubated with an excess of immunizing peptide. These results indicate that the antibody specifically recognizes FGFR-1. (D) low and (E) high magnification of section from control case YC1 demonstrating the exclusion of staining over the nuclei (panel D) and some surface staining (panel E). The majority of immunoreactivity is cytoplasmic, although the higher magnification panel (E) does indicate that some immunoreactivity appears surface localized. (F) Representative section of FGFR-1 immunoreactivity in an elderly control case (OC3). A similar pattern of immunoreactivity to the young control case can be observed. (G) Representative result showing FGFR-1 immunoreactivity in a section from a Parkinson's disease case (PD6). In this section it can be seen that some cells show strong immunoreactivity (arrowhead), which is an example of 2+ used in the rating scale, while adjacent ones have much weaker staining (arrow), which is an example of 1+ used in the rating scale. (H) Representative result showing the pattern of FGFR-1 immunoreactivity, using the monoclonal antibody, in a section from a normal case. Similar, though weaker, staining of SN DA neurons, compared to that obtained with the polyclonal antibody can be observed. (I) Section of SN showing prominent FGFR-1 immunoreactivity in cells with the profile of reactive astrocytes. Bar represents 50 μm in all figures, except panel D (25 μm).</note><note type="content">Table 1: Description of cases used in study</note><note type="content">Table 2: Summary of measurement of FGFR-1 immunoreactivity in human SN samples</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases</title><author xml:id="author-0000"><persName><forename type="first">Douglas G</forename><surname>Walker</surname></persName><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>1Present address: Sun Health Research Institute, Sun City, AZ, USA.</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Kazuhiro</forename><surname>Terai</surname></persName><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>2Present address: Yamanouchi Pharmaceutical Company, Japan.</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Akinori</forename><surname>Matsuo</surname></persName><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>3Present address: Department of Neurology, Kyoto University, Japan.</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Thomas G</forename><surname>Beach</surname></persName><affiliation>Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>4Present address: Sun Health Research Institute, Sun City, AZ, USA.</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Edith G</forename><surname>McGeer</surname></persName><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Patrick L</forename><surname>McGeer</surname></persName><email>mcgeerpl@unixg.ubc.ca</email><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation></author><idno type="istex">2E7AC6F53C260874E27058A3EF0823895208CCBC</idno><idno type="DOI">10.1016/S0006-8993(98)00132-2</idno><idno type="PII">S0006-8993(98)00132-2</idno><idno type="ArticleID">14466</idno></analytic><monogr><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="pISSN">0006-8993</idno><idno type="PII">S0006-8993(00)X0162-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">794</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="181">181</biblScope><biblScope unit="page" to="187">187</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Dopaminergic</term></item><item><term>Cell death</term></item><item><term>Neurodegeneration</term></item><item><term>Tyrosine kinase</term></item><item><term>Neuron</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/2E7AC6F53C260874E27058A3EF0823895208CCBC/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>BRES</jid><aid>14466</aid><ce:pii>S0006-8993(98)00132-2</ce:pii><ce:doi>10.1016/S0006-8993(98)00132-2</ce:doi><ce:copyright year="1998" type="full-transfer">Elsevier Science B.V.</ce:copyright></item-info><head><ce:dochead><ce:textfn>Research report</ce:textfn></ce:dochead><ce:title>Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases</ce:title><ce:author-group><ce:author><ce:given-name>Douglas G</ce:given-name><ce:surname>Walker</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Kazuhiro</ce:given-name><ce:surname>Terai</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="FN2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Akinori</ce:given-name><ce:surname>Matsuo</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="FN3"><ce:sup loc="post">3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Thomas G</ce:given-name><ce:surname>Beach</ce:surname><ce:cross-ref refid="AFF2">b</ce:cross-ref><ce:cross-ref refid="FN4"><ce:sup loc="post">4</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Edith G</ce:given-name><ce:surname>McGeer</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref></ce:author><ce:author><ce:given-name>Patrick L</ce:given-name><ce:surname>McGeer</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada. Fax: +1-604-822-7086; E-mail: mcgeerpl@unixg.ubc.ca</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Present address: Sun Health Research Institute, Sun City, AZ, USA.</ce:note-para></ce:footnote><ce:footnote id="FN2"><ce:label>2</ce:label><ce:note-para>Present address: Yamanouchi Pharmaceutical Company, Japan.</ce:note-para></ce:footnote><ce:footnote id="FN3"><ce:label>3</ce:label><ce:note-para>Present address: Department of Neurology, Kyoto University, Japan.</ce:note-para></ce:footnote><ce:footnote id="FN4"><ce:label>4</ce:label><ce:note-para>Present address: Sun Health Research Institute, Sun City, AZ, USA.</ce:note-para></ce:footnote></ce:author-group><ce:date-accepted day="27" month="1" year="1998"></ce:date-accepted><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0040">The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Dopaminergic</ce:text></ce:keyword><ce:keyword><ce:text>Cell death</ce:text></ce:keyword><ce:keyword><ce:text>Neurodegeneration</ce:text></ce:keyword><ce:keyword><ce:text>Tyrosine kinase</ce:text></ce:keyword><ce:keyword><ce:text>Neuron</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases</title></titleInfo><name type="personal"><namePart type="given">Douglas G</namePart><namePart type="family">Walker</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>1Present address: Sun Health Research Institute, Sun City, AZ, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazuhiro</namePart><namePart type="family">Terai</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>2Present address: Yamanouchi Pharmaceutical Company, Japan.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Akinori</namePart><namePart type="family">Matsuo</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>3Present address: Department of Neurology, Kyoto University, Japan.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas G</namePart><namePart type="family">Beach</namePart><affiliation>Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>4Present address: Sun Health Research Institute, Sun City, AZ, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Edith G</namePart><namePart type="family">McGeer</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patrick L</namePart><namePart type="family">McGeer</namePart><affiliation>Kinsmen Laboratory of Neurological Research, Department of Psychiatry and Neurodegenerative Disease Centre, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3</affiliation><affiliation>Corresponding author. Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada. Fax: +1-604-822-7086; E-mail: mcgeerpl@unixg.ubc.ca</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.</abstract><note type="content">Section title: Research report</note><note type="content">Fig. 1: (A) Strong FGFR-1 immunoreactivity can be demonstrated in pigmented SN dopaminergic neurons in a tissue section from a young control case (YC2). Section was stained with the polyclonal antibody to FGFR-1. (B) Parallel section to that demonstrated in panel A. The antibody used was preabsorbed with an excess of the immunizing peptide before the tissue incubation stage. Notice that the immunoreactivity demonstrated in the SN DA neurons in panel A has been abolished. (C) Immunoblot analyses of membrane extract derived from the SN of a control case. Lane a) demonstrates two main bands, with molecular weights of approximately 130–140 kD. They appear to represent FGFR-1 with three Ig domains. Lane b) shows the results of a parallel section of membrane to that in lane a) except that the antibody had been preincubated with an excess of immunizing peptide. These results indicate that the antibody specifically recognizes FGFR-1. (D) low and (E) high magnification of section from control case YC1 demonstrating the exclusion of staining over the nuclei (panel D) and some surface staining (panel E). The majority of immunoreactivity is cytoplasmic, although the higher magnification panel (E) does indicate that some immunoreactivity appears surface localized. (F) Representative section of FGFR-1 immunoreactivity in an elderly control case (OC3). A similar pattern of immunoreactivity to the young control case can be observed. (G) Representative result showing FGFR-1 immunoreactivity in a section from a Parkinson's disease case (PD6). In this section it can be seen that some cells show strong immunoreactivity (arrowhead), which is an example of 2+ used in the rating scale, while adjacent ones have much weaker staining (arrow), which is an example of 1+ used in the rating scale. (H) Representative result showing the pattern of FGFR-1 immunoreactivity, using the monoclonal antibody, in a section from a normal case. Similar, though weaker, staining of SN DA neurons, compared to that obtained with the polyclonal antibody can be observed. (I) Section of SN showing prominent FGFR-1 immunoreactivity in cells with the profile of reactive astrocytes. Bar represents 50 μm in all figures, except panel D (25 μm).</note><note type="content">Table 1: Description of cases used in study</note><note type="content">Table 2: Summary of measurement of FGFR-1 immunoreactivity in human SN samples</note><subject lang="en"><genre>Keywords</genre><topic>Dopaminergic</topic><topic>Cell death</topic><topic>Neurodegeneration</topic><topic>Tyrosine kinase</topic><topic>Neuron</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>BRES</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19980601</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0162-X</identifier><part><date>19980601</date><detail type="volume"><number>794</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>181</start><end>368</end></extent><extent unit="pages"><start>181</start><end>187</end></extent></part></relatedItem><identifier type="istex">2E7AC6F53C260874E27058A3EF0823895208CCBC</identifier><identifier type="DOI">10.1016/S0006-8993(98)00132-2</identifier><identifier type="PII">S0006-8993(98)00132-2</identifier><identifier type="ArticleID">14466</identifier><accessCondition type="use and reproduction" contentType="copyright">©1998 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science B.V., ©1998</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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