Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth
Identifieur interne : 000616 ( Main/Corpus ); précédent : 000615; suivant : 000617Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth
Auteurs : Bettina A. Buhren ; Marcia Gasis ; Bernard Thorens ; Hans Werner Müller ; Frank BosseSource :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2009-06.
English descriptors
Abstract
Glucose‐dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up‐regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion‐induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT‐PCR. Our results clearly identified lesion‐induced as well as tissue type‐specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane‐associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type‐specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR‐deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR‐deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild‐type mice. © 2009 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.22001
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Buhren</name><affiliation><mods:affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gasis, Marcia" sort="Gasis, Marcia" uniqKey="Gasis M" first="Marcia" last="Gasis">Marcia Gasis</name><affiliation><mods:affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Thorens, Bernard" sort="Thorens, Bernard" uniqKey="Thorens B" first="Bernard" last="Thorens">Bernard Thorens</name><affiliation><mods:affiliation>Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Muller, Hans Werner" sort="Muller, Hans Werner" uniqKey="Muller H" first="Hans Werner" last="Müller">Hans Werner Müller</name><affiliation><mods:affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bosse, Frank" sort="Bosse, Frank" uniqKey="Bosse F" first="Frank" last="Bosse">Frank Bosse</name><affiliation><mods:affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1002/jnr.22001</idno><idno type="url">https://api.istex.fr/document/DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000616</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth</title><author><name sortKey="Buhren, Bettina A" sort="Buhren, Bettina A" uniqKey="Buhren B" first="Bettina A." last="Buhren">Bettina A. 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Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-06">2009-06</date><biblScope unit="volume">87</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1858">1858</biblScope><biblScope unit="page" to="1870">1870</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478</idno><idno type="DOI">10.1002/jnr.22001</idno><idno type="ArticleID">JNR22001</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>dorsal root ganglia</term><term>glial cell, axons</term><term>nerve injury</term><term>neuropeptides</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glucose‐dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up‐regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion‐induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT‐PCR. Our results clearly identified lesion‐induced as well as tissue type‐specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane‐associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type‐specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR‐deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR‐deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild‐type mice. © 2009 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Bettina A. Buhren</name><affiliations><json:string>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Marcia Gasis</name><affiliations><json:string>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Bernard Thorens</name><affiliations><json:string>Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland</json:string></affiliations></json:item><json:item><name>Hans Werner Müller</name><affiliations><json:string>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Frank Bosse</name><affiliations><json:string>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>nerve injury</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dorsal root ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropeptides</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glial cell, axons</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Glucose‐dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up‐regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion‐induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT‐PCR. Our results clearly identified lesion‐induced as well as tissue type‐specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane‐associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type‐specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR‐deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR‐deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild‐type mice. © 2009 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.988</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1813</abstractCharCount><pdfWordCount>7926</pdfWordCount><pdfCharCount>51032</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>249</abstractWordCount></qualityIndicators><title>Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth</title><genre><json:string>article</json:string></genre><host><volume>87</volume><pages><total>13</total><last>1870</last><first>1858</first></pages><issn><json:string>0360-4012</json:string></issn><issue>8</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1097-4547</json:string></eissn><title>Journal of Neuroscience Research</title><doi><json:string>10.1002/(ISSN)1097-4547</json:string></doi></host><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/jnr.22001</json:string></doi><id>DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2009</date></publicationStmt><notesStmt><note>Deutsche Forschungsgemeinschaft - No. SFB 590 TP C2; No. GRK 1033;</note><note>Centre for Biological and Medical Research (BMFZ), University of Düsseldorf</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth</title><author><persName><forename type="first">Bettina A.</forename><surname>Buhren</surname></persName><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Marcia</forename><surname>Gasis</surname></persName><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Bernard</forename><surname>Thorens</surname></persName><affiliation>Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland</affiliation></author><author><persName><forename type="first">Hans Werner</forename><surname>Müller</surname></persName><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Frank</forename><surname>Bosse</surname></persName><note type="correspondence"><p>Correspondence: Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Moorenstr. 5, D‐40225 Düsseldorf, Germany</p></note><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation></author></analytic><monogr><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. 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Previously, we demonstrated a significant up‐regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion‐induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT‐PCR. Our results clearly identified lesion‐induced as well as tissue type‐specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane‐associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type‐specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR‐deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR‐deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild‐type mice. © 2009 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>nerve injury</term></item><item><term>dorsal root ganglia</term></item><item><term>neuropeptides</term></item><item><term>glial cell, axons</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-03-14">Received</change><change when="2008-11-16">Registration</change><change when="2009-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4547</doi><issn type="print">0360-4012</issn><issn type="electronic">1097-4547</issn><idGroup><id type="product" value="JNR"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF NEUROSCIENCE RESEARCH">Journal of Neuroscience Research</title><title type="short">J. 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Previously, we demonstrated a significant up‐regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion‐induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT‐PCR. Our results clearly identified lesion‐induced as well as tissue type‐specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane‐associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type‐specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR‐deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR‐deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild‐type mice. © 2009 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Lesion‐Affected GIP/GIPR Expression in the PNS and CNS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Glucose‐dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion‐affected expression, and impaired regenerative axonal growth</title></titleInfo><name type="personal"><namePart type="given">Bettina A.</namePart><namePart type="family">Buhren</namePart><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marcia</namePart><namePart type="family">Gasis</namePart><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bernard</namePart><namePart type="family">Thorens</namePart><affiliation>Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans Werner</namePart><namePart type="family">Müller</namePart><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frank</namePart><namePart type="family">Bosse</namePart><affiliation>Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Düsseldorf, Germany</affiliation><description>Correspondence: Molecular Neurobiology Laboratory, Department of Neurology, Heinrich‐Heine‐University of Düsseldorf, Moorenstr. 5, D‐40225 Düsseldorf, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-06</dateIssued><dateCaptured encoding="w3cdtf">2008-03-14</dateCaptured><dateValid encoding="w3cdtf">2008-11-16</dateValid><copyrightDate encoding="w3cdtf">2009</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">9</extent><extent unit="references">53</extent><extent unit="words">8326</extent></physicalDescription><abstract lang="en">Glucose‐dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up‐regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion‐induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT‐PCR. Our results clearly identified lesion‐induced as well as tissue type‐specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane‐associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type‐specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR‐deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR‐deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild‐type mice. © 2009 Wiley‐Liss, Inc.</abstract><note type="funding">Deutsche Forschungsgemeinschaft - No. SFB 590 TP C2; No. GRK 1033; </note><note type="funding">Centre for Biological and Medical Research (BMFZ), University of Düsseldorf</note><subject lang="en"><genre>Keywords</genre><topic>nerve injury</topic><topic>dorsal root ganglia</topic><topic>neuropeptides</topic><topic>glial cell, axons</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroscience Research</title></titleInfo><titleInfo type="abbreviated"><title>J. Neurosci. Res.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0360-4012</identifier><identifier type="eISSN">1097-4547</identifier><identifier type="DOI">10.1002/(ISSN)1097-4547</identifier><identifier type="PublisherID">JNR</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1858</start><end>1870</end><total>13</total></extent></part></relatedItem><identifier type="istex">DFEDC9594B8305C8CCF6B69C2D8FDFA9716B2478</identifier><identifier type="DOI">10.1002/jnr.22001</identifier><identifier type="ArticleID">JNR22001</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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