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Normal muscle regeneration requires tight control of muscle cell fusion by tetraspanins CD9 and CD81

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  • Stéphanie Charrin

    (Inserm, 14 rue Paul Vaillant Couturier
    Université Paris-Sud, Institut André Lwoff, 14 rue Paul Vaillant Couturier)

  • Mathilde Latil

    (Histopathologie Humaine et Modèles Animaux, Institut Pasteur, 28 rue du Dr Roux
    Université Versailles Saint Quentin en Yvelines UVSQ, faculté de médecine, 55 Avenue de Paris
    Université Paris Est Créteil UPEC, 61 Avenue du Général de Gaulle)

  • Sabrina Soave

    (Inserm, 14 rue Paul Vaillant Couturier
    Université Paris-Sud, Institut André Lwoff, 14 rue Paul Vaillant Couturier)

  • Anna Polesskaya

    (CNRS FRE 3377, CEA Saclay
    Université Paris-Sud)

  • Fabrice Chrétien

    (Histopathologie Humaine et Modèles Animaux, Institut Pasteur, 28 rue du Dr Roux
    Université Versailles Saint Quentin en Yvelines UVSQ, faculté de médecine, 55 Avenue de Paris
    Service d’Anatomie Pathologique et de Médecine légale, Hôpital Raymond Poincaré, Assistance Publique Hôpitaux de Paris AP-HP, 104 Boulevard Raymond Poincaré)

  • Claude Boucheix

    (Inserm, 14 rue Paul Vaillant Couturier
    Université Paris-Sud, Institut André Lwoff, 14 rue Paul Vaillant Couturier)

  • Eric Rubinstein

    (Inserm, 14 rue Paul Vaillant Couturier
    Université Paris-Sud, Institut André Lwoff, 14 rue Paul Vaillant Couturier)

Abstract

Skeletal muscle regeneration after injury follows a remarkable sequence of synchronized events. However, the mechanisms regulating the typical organization of the regenerating muscle at different stages remain largely unknown. Here we show that muscle regeneration in mice lacking either CD9 or CD81 is abnormal and characterized by the formation of discrete giant dystrophic myofibres, which form more quickly in the absence of both tetraspanins. We also show that, in myoblasts, these two tetraspanins associate with the immunoglobulin domain molecule CD9P-1 (EWI-F/FPRP), and that grafting of CD9P-1-depleted myoblasts in regenerating muscles also leads to abnormal regeneration. In vitro myotubes lacking CD9P-1 or both CD9 and CD81 fuse with a higher frequency than normal myotubes. Our study unveils a mechanism preventing inappropriate fusion of myotubes that has an important role in the restitution of normal muscle architecture during muscle regeneration.

Suggested Citation

  • Stéphanie Charrin & Mathilde Latil & Sabrina Soave & Anna Polesskaya & Fabrice Chrétien & Claude Boucheix & Eric Rubinstein, 2013. "Normal muscle regeneration requires tight control of muscle cell fusion by tetraspanins CD9 and CD81," Nature Communications, Nature, vol. 4(1), pages 1-12, June.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2675
    DOI: 10.1038/ncomms2675
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