Unilateral induction of progenitors in the spinal cord of hSOD1(G93A) transgenic rats correlates with an asymmetrical hind limb paralysis
Transgenic rats expressing a mutated form of the human Cu/Zn superoxide dismutase (hSOD1(G93A)) develop an amyotrophic lateral sclerosis (ALS)-like phenotype, including motor neurone degeneration and reactive gliosis in the spinal cord. This study aimed at examining the presence of endogenous neural...
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Veröffentlicht in: | Neuroscience letters 2006-06, Vol.401 (1-2), p.25-29 |
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description | Transgenic rats expressing a mutated form of the human Cu/Zn superoxide dismutase (hSOD1(G93A)) develop an amyotrophic lateral sclerosis (ALS)-like phenotype, including motor neurone degeneration and reactive gliosis in the spinal cord. This study aimed at examining the presence of endogenous neural progenitors in the lumbar spinal cord of these rats at the end-stage of the disease. Immunohistochemical data clearly demonstrated the induced expression of the stem cell factor reported as a chemoattractant and survival factor for neural stem cells as well as nestin (neuro-epithelial stem cell intermediate filament) in the spinal cord sections. While the stem cell factor immunolabelling appeared diffuse throughout the gray matter, nestin labelling was restricted to clusters within the ventral horn. Interestingly, as paralysis regularly develops asymmetrically, induction of nestin was only detected on the ipsilateral side of the predominant symptoms. Finally, immunohistochemical detection of the stem cell factor receptor (c-Kit) revealed its specific induction which coincided with nestin immunolabelling. Together, these results are indicative of endogenous recruitment of neural progenitors within lesioned tissues and could support the development of treatments involving endogenous or exogenous stem cells. |
doi_str_mv | 10.1016/j.neulet.2006.02.060 |
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This study aimed at examining the presence of endogenous neural progenitors in the lumbar spinal cord of these rats at the end-stage of the disease. Immunohistochemical data clearly demonstrated the induced expression of the stem cell factor reported as a chemoattractant and survival factor for neural stem cells as well as nestin (neuro-epithelial stem cell intermediate filament) in the spinal cord sections. While the stem cell factor immunolabelling appeared diffuse throughout the gray matter, nestin labelling was restricted to clusters within the ventral horn. Interestingly, as paralysis regularly develops asymmetrically, induction of nestin was only detected on the ipsilateral side of the predominant symptoms. Finally, immunohistochemical detection of the stem cell factor receptor (c-Kit) revealed its specific induction which coincided with nestin immunolabelling. Together, these results are indicative of endogenous recruitment of neural progenitors within lesioned tissues and could support the development of treatments involving endogenous or exogenous stem cells.</description><identifier>ISSN: 0304-3940</identifier><identifier>DOI: 10.1016/j.neulet.2006.02.060</identifier><identifier>PMID: 16540243</identifier><language>eng</language><publisher>Ireland</publisher><subject>Amyotrophic Lateral Sclerosis - genetics ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - physiopathology ; Animals ; Animals, Genetically Modified ; Cell Differentiation - genetics ; Cell Movement - genetics ; Disease Models, Animal ; Functional Laterality - genetics ; Hindlimb - innervation ; Hindlimb - physiopathology ; Humans ; Immunohistochemistry ; Intermediate Filament Proteins - metabolism ; Motor Neurons - metabolism ; Nerve Regeneration - genetics ; Nerve Tissue Proteins - metabolism ; Nestin ; Neurons - metabolism ; Paralysis - genetics ; Paralysis - metabolism ; Paralysis - physiopathology ; Proto-Oncogene Proteins c-kit - metabolism ; Rats ; Recovery of Function - genetics ; Spinal Cord - cytology ; Spinal Cord - metabolism ; Spinal Cord - physiopathology ; Stem Cell Factor - metabolism ; Stem Cells - cytology ; Stem Cells - metabolism ; Superoxide Dismutase - genetics ; Superoxide Dismutase-1</subject><ispartof>Neuroscience letters, 2006-06, Vol.401 (1-2), p.25-29</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16540243$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Hemptinne, Isabelle</creatorcontrib><creatorcontrib>Boucherie, Cédric</creatorcontrib><creatorcontrib>Pochet, Roland</creatorcontrib><creatorcontrib>Bantubungi, Kadiombo</creatorcontrib><creatorcontrib>Schiffmann, Serge N</creatorcontrib><creatorcontrib>Maloteaux, Jean-Marie</creatorcontrib><creatorcontrib>Hermans, Emmanuel</creatorcontrib><title>Unilateral induction of progenitors in the spinal cord of hSOD1(G93A) transgenic rats correlates with an asymmetrical hind limb paralysis</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Transgenic rats expressing a mutated form of the human Cu/Zn superoxide dismutase (hSOD1(G93A)) develop an amyotrophic lateral sclerosis (ALS)-like phenotype, including motor neurone degeneration and reactive gliosis in the spinal cord. This study aimed at examining the presence of endogenous neural progenitors in the lumbar spinal cord of these rats at the end-stage of the disease. Immunohistochemical data clearly demonstrated the induced expression of the stem cell factor reported as a chemoattractant and survival factor for neural stem cells as well as nestin (neuro-epithelial stem cell intermediate filament) in the spinal cord sections. While the stem cell factor immunolabelling appeared diffuse throughout the gray matter, nestin labelling was restricted to clusters within the ventral horn. Interestingly, as paralysis regularly develops asymmetrically, induction of nestin was only detected on the ipsilateral side of the predominant symptoms. Finally, immunohistochemical detection of the stem cell factor receptor (c-Kit) revealed its specific induction which coincided with nestin immunolabelling. Together, these results are indicative of endogenous recruitment of neural progenitors within lesioned tissues and could support the development of treatments involving endogenous or exogenous stem cells.</description><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - physiopathology</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Movement - genetics</subject><subject>Disease Models, Animal</subject><subject>Functional Laterality - genetics</subject><subject>Hindlimb - innervation</subject><subject>Hindlimb - physiopathology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Intermediate Filament Proteins - metabolism</subject><subject>Motor Neurons - metabolism</subject><subject>Nerve Regeneration - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nestin</subject><subject>Neurons - metabolism</subject><subject>Paralysis - genetics</subject><subject>Paralysis - metabolism</subject><subject>Paralysis - physiopathology</subject><subject>Proto-Oncogene Proteins c-kit - metabolism</subject><subject>Rats</subject><subject>Recovery of Function - genetics</subject><subject>Spinal Cord - cytology</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - physiopathology</subject><subject>Stem Cell Factor - metabolism</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase-1</subject><issn>0304-3940</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo10L9OwzAQBnAPIFoKb4CQJwRDwvlf0oxVgYJUqQN0jtzEJq4SJ9iOUB-Bt8YVZbrhfvo-3SF0QyAlQLLHfWrV2KqQUoAsBZpCBmdoCgx4wgoOE3Tp_R4ABBH8Ak1IJjhQzqboZ2tNK4NyssXG1mMVTG9xr_Hg-k9lTeidjwscGoX9YGxkVe_qo2jeN0_kflWwxQMOTlp_9BV2MvijceqY6_G3CQ2WFkt_6DoVnKliRhO7cGu6HR5krD5446_QuZatV9enOUPbl-eP5Wuy3qzelot1MlAoQiI45YXWRHKuKeFzyvOC1kITOmecVFLqjBZUi53mXDGtK6hyQkXUc6G0ytkM3f3lxgu_RuVD2RlfqbaVVvWjL7O8yIUgJMLbExx3narLwZlOukP5_zz2C3sLcso</recordid><startdate>20060619</startdate><enddate>20060619</enddate><creator>de Hemptinne, Isabelle</creator><creator>Boucherie, Cédric</creator><creator>Pochet, Roland</creator><creator>Bantubungi, Kadiombo</creator><creator>Schiffmann, Serge N</creator><creator>Maloteaux, Jean-Marie</creator><creator>Hermans, Emmanuel</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20060619</creationdate><title>Unilateral induction of progenitors in the spinal cord of hSOD1(G93A) transgenic rats correlates with an asymmetrical hind limb paralysis</title><author>de Hemptinne, Isabelle ; Boucherie, Cédric ; Pochet, Roland ; Bantubungi, Kadiombo ; Schiffmann, Serge N ; Maloteaux, Jean-Marie ; Hermans, Emmanuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p209t-54249ff1a44f214824792d5f128341caaf6292f5bf44e3ffc0c712544f85efe73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Amyotrophic Lateral Sclerosis - physiopathology</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Movement - genetics</topic><topic>Disease Models, Animal</topic><topic>Functional Laterality - genetics</topic><topic>Hindlimb - innervation</topic><topic>Hindlimb - physiopathology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Intermediate Filament Proteins - metabolism</topic><topic>Motor Neurons - metabolism</topic><topic>Nerve Regeneration - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nestin</topic><topic>Neurons - metabolism</topic><topic>Paralysis - genetics</topic><topic>Paralysis - metabolism</topic><topic>Paralysis - physiopathology</topic><topic>Proto-Oncogene Proteins c-kit - metabolism</topic><topic>Rats</topic><topic>Recovery of Function - genetics</topic><topic>Spinal Cord - cytology</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - physiopathology</topic><topic>Stem Cell Factor - metabolism</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - metabolism</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Hemptinne, Isabelle</creatorcontrib><creatorcontrib>Boucherie, Cédric</creatorcontrib><creatorcontrib>Pochet, Roland</creatorcontrib><creatorcontrib>Bantubungi, Kadiombo</creatorcontrib><creatorcontrib>Schiffmann, Serge N</creatorcontrib><creatorcontrib>Maloteaux, Jean-Marie</creatorcontrib><creatorcontrib>Hermans, Emmanuel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Hemptinne, Isabelle</au><au>Boucherie, Cédric</au><au>Pochet, Roland</au><au>Bantubungi, Kadiombo</au><au>Schiffmann, Serge N</au><au>Maloteaux, Jean-Marie</au><au>Hermans, Emmanuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Unilateral induction of progenitors in the spinal cord of hSOD1(G93A) transgenic rats correlates with an asymmetrical hind limb paralysis</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2006-06-19</date><risdate>2006</risdate><volume>401</volume><issue>1-2</issue><spage>25</spage><epage>29</epage><pages>25-29</pages><issn>0304-3940</issn><abstract>Transgenic rats expressing a mutated form of the human Cu/Zn superoxide dismutase (hSOD1(G93A)) develop an amyotrophic lateral sclerosis (ALS)-like phenotype, including motor neurone degeneration and reactive gliosis in the spinal cord. This study aimed at examining the presence of endogenous neural progenitors in the lumbar spinal cord of these rats at the end-stage of the disease. Immunohistochemical data clearly demonstrated the induced expression of the stem cell factor reported as a chemoattractant and survival factor for neural stem cells as well as nestin (neuro-epithelial stem cell intermediate filament) in the spinal cord sections. While the stem cell factor immunolabelling appeared diffuse throughout the gray matter, nestin labelling was restricted to clusters within the ventral horn. Interestingly, as paralysis regularly develops asymmetrically, induction of nestin was only detected on the ipsilateral side of the predominant symptoms. Finally, immunohistochemical detection of the stem cell factor receptor (c-Kit) revealed its specific induction which coincided with nestin immunolabelling. Together, these results are indicative of endogenous recruitment of neural progenitors within lesioned tissues and could support the development of treatments involving endogenous or exogenous stem cells.</abstract><cop>Ireland</cop><pmid>16540243</pmid><doi>10.1016/j.neulet.2006.02.060</doi><tpages>5</tpages></addata></record> |
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subjects | Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - physiopathology Animals Animals, Genetically Modified Cell Differentiation - genetics Cell Movement - genetics Disease Models, Animal Functional Laterality - genetics Hindlimb - innervation Hindlimb - physiopathology Humans Immunohistochemistry Intermediate Filament Proteins - metabolism Motor Neurons - metabolism Nerve Regeneration - genetics Nerve Tissue Proteins - metabolism Nestin Neurons - metabolism Paralysis - genetics Paralysis - metabolism Paralysis - physiopathology Proto-Oncogene Proteins c-kit - metabolism Rats Recovery of Function - genetics Spinal Cord - cytology Spinal Cord - metabolism Spinal Cord - physiopathology Stem Cell Factor - metabolism Stem Cells - cytology Stem Cells - metabolism Superoxide Dismutase - genetics Superoxide Dismutase-1 |
title | Unilateral induction of progenitors in the spinal cord of hSOD1(G93A) transgenic rats correlates with an asymmetrical hind limb paralysis |
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