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
Hauptverfasser: Ates, Kenan, Yang, Shi Yu, Orrell, Richard W., Sinanan, Andrea C.M., Simons, Paul, Solomon, Andrew, Beech, Steven, Goldspink, Geoffrey, Lewis, Mark P.
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container_end_page 2732
container_issue 14
container_start_page 2727
container_title FEBS letters
container_volume 581
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.</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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