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Published online October 22, 2007
doi:10.1083/jcb.200701027
The Journal of Cell Biology, Vol. 179, No. 2, 305-319
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Deponti et al.
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Article

 Necdin mediates skeletal muscle regeneration by promoting myoblast survival and differentiation

Daniela Deponti1,2, Stéphanie François3, Silvia Baesso4, Clara Sciorati4, Anna Innocenzi4, Vania Broccoli4, Françoise Muscatelli5, Raffaella Meneveri3, Emilio Clementi2,6, Giulio Cossu4,7, and Silvia Brunelli3,4

1 Department of Histology and Medical Embryology, University of Roma-La Sapienza, 00161 Rome, Italy
2 E. Medea Scientific Institute, 23842 Bosisio Parini, Italy
3 Department of Experimental Medicine, University of Milano-Bicocca, 20052 Monza, Italy
4 Stem Cell Research Institute, San Raffaele Scientific Institute, 20132 Milan, Italy
5 Neurogenèse et Morphogenèse dans le Développement et chez l'Adulte, Centre National de la Recherche Scientifique UMR 6156, Institut de Biologie du Développement de Marseille, 13288 Marseille Cedex 9, France
6 Department of Preclinical Sciences, LITA-Vialba, University of Milan, 20157 Milan, Italy
7 Department of Biology, University of Milan, 20130 Milan, Italy

Correspondence to Silvia Brunelli: silvia.brunelli{at}unimib.it; or Giulio Cossu: giulio.cossu{at}unimi.it

Regeneration of muscle fibers that are lost during pathological muscle degeneration or after injuries is sustained by the production of new myofibers. An important cell type involved in muscle regeneration is the satellite cell. Necdin is a protein expressed in satellite cell–derived myogenic precursors during perinatal growth. However, its function in myogenesis is not known. We compare transgenic mice that overexpress necdin in skeletal muscle with both wild-type and necdin null mice. After muscle injury the necdin null mice show a considerable defect in muscle healing, whereas mice that overexpress necdin show a substantial increase in myofiber regeneration. We also find that in muscle, necdin increases myogenin expression, accelerates differentiation, and counteracts myoblast apoptosis. Collectively, these data clarify the function and mechanism of necdin in skeletal muscle and show the importance of necdin in muscle regeneration.

Abbreviations used in this paper: CAT, chloramphenicol acetyltransferase; CTX, cardiotoxin; GAPDH, antiglyceraldehyde 3-phosphate dehydrogenase; H&E, hematoxylin and eosin; MyLC, myosin light chain; MRF, myogenic regulatory factor; MyHC; myosin heavy chain; P, postnatal day; PCNA, proliferating cell nuclear antigen; TA, tibialis anterior; wt, wild type; XSA, cross-sectional area.


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