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RESEARCH COMMUNICATION

Essential and separable roles for Syndecan-3 and Syndecan-4 in skeletal muscle development and regeneration

¹ Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Boulder, Colorado 80309, USA; ² Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA; ³ Neuroscience Center, Department of Biosciences, and Institute of Biotechnology, University of Helsinki, Helsinki FIN-00014, Finland; ⁴ Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA

Syndecan-3 and syndecan-4 function as coreceptors for tyrosine kinases and in cell adhesion. Syndecan-3^-/- mice exhibit a novel form of muscular dystrophy characterized by impaired locomotion, fibrosis, and hyperplasia of myonuclei and satellite cells. Explanted syndecan-3^-/- satellite cells mislocalize MyoD, differentiate aberrantly, and exhibit a general increase in overall tyrosine phosphorylation. Following induced regeneration, the hyperplastic phenotype is recapitulated. While there are fewer apparent defects in syndecan-4^-/- muscle, explanted satellite cells are deficient in activation, proliferation, MyoD expression, myotube fusion, and differentiation. Further, syndecan-4^-/- satellite cells fail to reconstitute damaged muscle, suggesting a unique requirement for syndecan-4 in satellite cell function.

[Keywords: Muscle regeneration; satellite cell; stem cell; myogenesis]

Received April 23, 2004; revised version accepted July 15, 2004.

Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1214204.

⁵ Corresponding author.
E-MAIL bradley.olwin{at}colorado.edu; FAX (303) 492-1587.

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