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TISSUE-SPECIFIC STEM CELLS

Galectin-1 Induces Skeletal Muscle Differentiation in Human Fetal Mesenchymal Stem Cells and Increases Muscle Regeneration

^aInstitute of Reproductive and Developmental Biology,
^bDepartment of Paediatrics, Imperial College London, Hammersmith Campus, London, United Kingdom;
^cDepartment of Anatomy, Brighton and Sussex Medical School, Falmer, Brighton, East Sussex, United Kingdom;
^dMuscle Cell Biology, Medical Research Council Clinical Sciences Centre, Imperial College London, London, United Kingdom;
^eFondazione Istituto di Ricovero e Cura a Carattere Scientifico Ospedale Maggiore Policlinico, Department of Neurological Sciences, Stem Cell Laboratory, University of Milan, Italy

Key Words. Mesenchymal stem cells • scid/mdx • Muscle differentiation • Galectin-1 • Fetal stem cells • Fetal • Myogenesis

Correspondence: Dr. Jerry Chan, MBB.Ch. MRCOG, Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore & National University Hospital, 5 Lower Kent Ridge Road, Singapore 119074. Telephone: +65-6772-4268; Fax: +65-6779-4753; e-mail: jerrychan{at}nus.edu.sg

Received on November 14, 2005; accepted for publication on April 28, 2006.

First published online in STEM CELLS EXPRESS  May 4, 2006.


Cell therapy for degenerative muscle diseases such as the muscular dystrophies requires a source of cells with the capacity to participate in the formation of new muscle fibers. We investigated the myogenic potential of human fetal mesenchymal stem cells (hfMSCs) using a variety of stimuli. The use of 5-azacytidine or steroids did not produce skeletal muscle differentiation, whereas myoblast-conditioned medium resulted in only 1%–2% of hfMSCs undergoing muscle differentiation. However, in the presence of galectin-1, 66.1% ± 5.7% of hfMSCs, but not adult bone marrow-derived mesenchymal stem cells, assumed a muscle phenotype, forming long, multinucleated fibers expressing both desmin and sarcomeric myosin via activation of muscle regulatory factors. Continuous exposure to galectin-1 resulted in more efficient muscle differentiation than pulsed exposure (62.3% vs. 39.1%; p < .001). When transplanted into regenerating murine muscle, galectin-1-exposed hfMSCs formed fourfold more human muscle fibers than nonstimulated hfMSCs (p = .008), with similar results obtained in a scid/mdx dystrophic mouse model. These data suggest that hfMSCs readily undergo muscle differentiation in response to galectin-1 through a stepwise progression similar to that which occurs during embryonic myogenesis. The high degree of myogenic conversion achieved by this method has relevance for the development of therapies for muscular dystrophies.

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