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

Stéphanie Charrin (), Mathilde Latil, Sabrina Soave, Anna Polesskaya, Fabrice Chrétien, Claude Boucheix and Eric Rubinstein
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Stéphanie Charrin: Inserm, 14 rue Paul Vaillant Couturier
Mathilde Latil: Histopathologie Humaine et Modèles Animaux, Institut Pasteur, 28 rue du Dr Roux
Sabrina Soave: Inserm, 14 rue Paul Vaillant Couturier
Anna Polesskaya: CNRS FRE 3377, CEA Saclay
Fabrice Chrétien: Histopathologie Humaine et Modèles Animaux, Institut Pasteur, 28 rue du Dr Roux
Claude Boucheix: Inserm, 14 rue Paul Vaillant Couturier
Eric Rubinstein: Inserm, 14 rue Paul Vaillant Couturier

Nature Communications, 2013, vol. 4, issue 1, 1-12

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms2675

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