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    ATP regulates the differentiation of mammalian skeletal muscle by activation of a P2X(5) receptor on satellite cells

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    106
    Author
    Ryten, M; Dunn, PM; Neary, JT; Burnstock, G
    Date
    2002-07-22
    Source Title
    The Journal of Cell Biology
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Burnstock, Geoffrey
    Affiliation
    Pharmacology and Therapeutics
    Metadata
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    Document Type
    Journal Article
    Citations
    Ryten, M., Dunn, P. M., Neary, J. T. & Burnstock, G. (2002). ATP regulates the differentiation of mammalian skeletal muscle by activation of a P2X(5) receptor on satellite cells. JOURNAL OF CELL BIOLOGY, 158 (2), pp.345-355. https://doi.org/10.1083/jcb.200202025.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259140
    DOI
    10.1083/jcb.200202025
    Abstract
    ATP is well known for its role as an intracellular energy source. However, there is increasing awareness of its role as an extracellular messenger molecule (Burnstock, 1997). Although evidence for the presence of receptors for extracellular ATP on skeletal myoblasts was first published in 1983 (Kolb and Wakelam), their physiological function has remained unclear. In this paper we used primary cultures of rat skeletal muscle satellite cells to investigate the role of purinergic signaling in muscle formation. Using immunocytochemistry, RT-PCR, and electrophysiology, we demonstrate that the ionotropic P2X5 receptor is present on satellite cells and that activation of a P2X receptor inhibits proliferation, stimulates expression of markers of muscle cell differentiation, including myogenin, p21, and myosin heavy chain, and increases the rate of myotube formation. Furthermore, we demonstrate that ATP application results in a significant and rapid increase in the phosphorylation of MAPKs, particularly p38, and that inhibition of p38 activity can prevent the effect of ATP on cell number. These results not only demonstrate the existence of a novel regulator of skeletal muscle differentiation, namely ATP, but also a new role for ionotropic P2X receptors in the control of cell fate.

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