The IGF-I splice variant MGF increases progenitor cells in ALS, dystrophic, and normal muscle
The effects of muscle splice variants of insulin-like growth factor I (IGF-I) on proliferation and differentiation were studied in human primary muscle cell cultures from healthy subjects as well as from muscular dystrophy and ALS patients. Although the initial numbers of mononucleated progenitor ce...
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Veröffentlicht in: | FEBS letters 2007-06, Vol.581 (14), p.2727-2732 |
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creator | Ates, Kenan Yang, Shi Yu Orrell, Richard W. Sinanan, Andrea C.M. Simons, Paul Solomon, Andrew Beech, Steven Goldspink, Geoffrey Lewis, Mark P. |
description | The effects of muscle splice variants of insulin-like growth factor I (IGF-I) on proliferation and differentiation were studied in human primary muscle cell cultures from healthy subjects as well as from muscular dystrophy and ALS patients. Although the initial numbers of mononucleated progenitor cells expressing desmin were lower in diseased muscle, the E domain peptide of IGF-IEc (MGF) significantly increased the numbers of progenitor cells in healthy and diseased muscle. IGF-I significantly enhances myogenic differentiation whereas MGF E peptide blocks this pathway, resulting in an increased progenitor (stem) cell pool and thus potentially facilitating repair and maintenance of this postmitotic tissue. |
doi_str_mv | 10.1016/j.febslet.2007.05.030 |
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Although the initial numbers of mononucleated progenitor cells expressing desmin were lower in diseased muscle, the E domain peptide of IGF-IEc (MGF) significantly increased the numbers of progenitor cells in healthy and diseased muscle. IGF-I significantly enhances myogenic differentiation whereas MGF E peptide blocks this pathway, resulting in an increased progenitor (stem) cell pool and thus potentially facilitating repair and maintenance of this postmitotic tissue.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2007.05.030</identifier><identifier>PMID: 17531227</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Adult ; ALS ; Alternative Splicing ; Antibodies, Monoclonal - pharmacology ; Cell Proliferation - drug effects ; Cells, Cultured ; Creatine Kinase - metabolism ; Desmin - analysis ; Dose-Response Relationship, Drug ; Humans ; Immunohistochemistry ; Insulin-like growth factor I ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - pharmacology ; Mechano growth factor ; Microscopy, Fluorescence ; Muscle stem ; Muscle, Skeletal - cytology ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - metabolism ; Muscular Atrophy - congenital ; Muscular Atrophy - metabolism ; Muscular Atrophy - pathology ; Muscular dystrophy ; Protein Isoforms - pharmacology ; Receptor, IGF Type 1 - immunology ; Receptor, IGF Type 1 - metabolism ; Satellite cells ; Stem Cells - cytology ; Stem Cells - drug effects ; Stem Cells - metabolism</subject><ispartof>FEBS letters, 2007-06, Vol.581 (14), p.2727-2732</ispartof><rights>2007 Federation of European Biochemical Societies</rights><rights>FEBS Letters 581 (2007) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5723-47315da9f5c27986ec7e28f26cbacb83560ed30b45365513baddd10fca45fa6a3</citedby><cites>FETCH-LOGICAL-c5723-47315da9f5c27986ec7e28f26cbacb83560ed30b45365513baddd10fca45fa6a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.febslet.2007.05.030$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014579307005583$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,1427,3537,27901,27902,45550,45551,46384,46808,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17531227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ates, Kenan</creatorcontrib><creatorcontrib>Yang, Shi Yu</creatorcontrib><creatorcontrib>Orrell, Richard W.</creatorcontrib><creatorcontrib>Sinanan, Andrea C.M.</creatorcontrib><creatorcontrib>Simons, Paul</creatorcontrib><creatorcontrib>Solomon, Andrew</creatorcontrib><creatorcontrib>Beech, Steven</creatorcontrib><creatorcontrib>Goldspink, Geoffrey</creatorcontrib><creatorcontrib>Lewis, Mark P.</creatorcontrib><title>The IGF-I splice variant MGF increases progenitor cells in ALS, dystrophic, and normal muscle</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>The effects of muscle splice variants of insulin-like growth factor I (IGF-I) on proliferation and differentiation were studied in human primary muscle cell cultures from healthy subjects as well as from muscular dystrophy and ALS patients. Although the initial numbers of mononucleated progenitor cells expressing desmin were lower in diseased muscle, the E domain peptide of IGF-IEc (MGF) significantly increased the numbers of progenitor cells in healthy and diseased muscle. IGF-I significantly enhances myogenic differentiation whereas MGF E peptide blocks this pathway, resulting in an increased progenitor (stem) cell pool and thus potentially facilitating repair and maintenance of this postmitotic tissue.</description><subject>Adult</subject><subject>ALS</subject><subject>Alternative Splicing</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Creatine Kinase - metabolism</subject><subject>Desmin - analysis</subject><subject>Dose-Response Relationship, Drug</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Mechano growth factor</subject><subject>Microscopy, Fluorescence</subject><subject>Muscle stem</subject><subject>Muscle, Skeletal - cytology</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscular Atrophy - congenital</subject><subject>Muscular Atrophy - metabolism</subject><subject>Muscular Atrophy - pathology</subject><subject>Muscular dystrophy</subject><subject>Protein Isoforms - pharmacology</subject><subject>Receptor, IGF Type 1 - immunology</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Satellite cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - metabolism</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU9v2zAMxYVhQ5t1_QgbdNqp9ijJsuzT0BZNGiDDDm2PhSBL9KrAfzLJ6ZBvPxkJsGN3Igg-Pj7wR8hnBjkDVn7b5i02scMp5wAqB5mDgHdkwSolMlGU1XuyAGBFJlUtzsnHGLeQ-orVZ-ScKSkY52pBnh9fkK5Xy2xN467zFumrCd4ME_2xWlI_2IAmYqS7MP7CwU9joBa7LqYRvd48XFF3iFMYdy_eXlEzODqMoTcd7ffRdviJfGhNF_HyVC_I0_Lu8fY-2_xcrW-vN5mViousUIJJZ-pWWq7qqkSrkFctL21jbFMJWQI6AU0hRSklE41xzjForSlka0ojLsjXo2-K-XuPcdK9j3NOM-C4j1pBusPL-k0hh6JWoKoklEehDWOMAVu9C7434aAZ6BmA3uoTAD0D0CB1ApD2vpwO7Jse3b-t08eT4P4o-OM7PPyfq17e3fCHmeYMExSAlJVIVt-PVphe--ox6Gg9DhadD2gn7Ub_Rtq_-sWuHA</recordid><startdate>20070612</startdate><enddate>20070612</enddate><creator>Ates, Kenan</creator><creator>Yang, Shi Yu</creator><creator>Orrell, Richard W.</creator><creator>Sinanan, Andrea C.M.</creator><creator>Simons, Paul</creator><creator>Solomon, Andrew</creator><creator>Beech, Steven</creator><creator>Goldspink, Geoffrey</creator><creator>Lewis, Mark P.</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20070612</creationdate><title>The IGF-I splice variant MGF increases progenitor cells in ALS, dystrophic, and normal muscle</title><author>Ates, Kenan ; Yang, Shi Yu ; Orrell, Richard W. ; Sinanan, Andrea C.M. ; Simons, Paul ; Solomon, Andrew ; Beech, Steven ; Goldspink, Geoffrey ; Lewis, Mark P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5723-47315da9f5c27986ec7e28f26cbacb83560ed30b45365513baddd10fca45fa6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>ALS</topic><topic>Alternative Splicing</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Creatine Kinase - metabolism</topic><topic>Desmin - analysis</topic><topic>Dose-Response Relationship, Drug</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Insulin-like growth factor I</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Insulin-Like Growth Factor I - pharmacology</topic><topic>Mechano growth factor</topic><topic>Microscopy, Fluorescence</topic><topic>Muscle stem</topic><topic>Muscle, Skeletal - cytology</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscular Atrophy - congenital</topic><topic>Muscular Atrophy - metabolism</topic><topic>Muscular Atrophy - pathology</topic><topic>Muscular dystrophy</topic><topic>Protein Isoforms - pharmacology</topic><topic>Receptor, IGF Type 1 - immunology</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Satellite cells</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ates, Kenan</creatorcontrib><creatorcontrib>Yang, Shi Yu</creatorcontrib><creatorcontrib>Orrell, Richard W.</creatorcontrib><creatorcontrib>Sinanan, Andrea C.M.</creatorcontrib><creatorcontrib>Simons, Paul</creatorcontrib><creatorcontrib>Solomon, Andrew</creatorcontrib><creatorcontrib>Beech, Steven</creatorcontrib><creatorcontrib>Goldspink, Geoffrey</creatorcontrib><creatorcontrib>Lewis, Mark P.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ates, Kenan</au><au>Yang, Shi Yu</au><au>Orrell, Richard W.</au><au>Sinanan, Andrea C.M.</au><au>Simons, Paul</au><au>Solomon, Andrew</au><au>Beech, Steven</au><au>Goldspink, Geoffrey</au><au>Lewis, Mark P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The IGF-I splice variant MGF increases progenitor cells in ALS, dystrophic, and normal muscle</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2007-06-12</date><risdate>2007</risdate><volume>581</volume><issue>14</issue><spage>2727</spage><epage>2732</epage><pages>2727-2732</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>The effects of muscle splice variants of insulin-like growth factor I (IGF-I) on proliferation and differentiation were studied in human primary muscle cell cultures from healthy subjects as well as from muscular dystrophy and ALS patients. Although the initial numbers of mononucleated progenitor cells expressing desmin were lower in diseased muscle, the E domain peptide of IGF-IEc (MGF) significantly increased the numbers of progenitor cells in healthy and diseased muscle. IGF-I significantly enhances myogenic differentiation whereas MGF E peptide blocks this pathway, resulting in an increased progenitor (stem) cell pool and thus potentially facilitating repair and maintenance of this postmitotic tissue.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>17531227</pmid><doi>10.1016/j.febslet.2007.05.030</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult ALS Alternative Splicing Antibodies, Monoclonal - pharmacology Cell Proliferation - drug effects Cells, Cultured Creatine Kinase - metabolism Desmin - analysis Dose-Response Relationship, Drug Humans Immunohistochemistry Insulin-like growth factor I Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - pharmacology Mechano growth factor Microscopy, Fluorescence Muscle stem Muscle, Skeletal - cytology Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Muscular Atrophy - congenital Muscular Atrophy - metabolism Muscular Atrophy - pathology Muscular dystrophy Protein Isoforms - pharmacology Receptor, IGF Type 1 - immunology Receptor, IGF Type 1 - metabolism Satellite cells Stem Cells - cytology Stem Cells - drug effects Stem Cells - metabolism |
title | The IGF-I splice variant MGF increases progenitor cells in ALS, dystrophic, and normal muscle |
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