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A correction to this article has been published: Galvez et al., J. Cell Biol. 175 (2) 361
A correction to this article has been published: Galvez et al., J. Cell Biol. 174 (4) 605
Published online 10 July 2006. doi:10.1083/jcb.200512085
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 174, Number 2, 231-243
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Article

Complete repair of dystrophic skeletal muscle by mesoangioblasts with enhanced migration ability



Beatriz G. Galvez1, Maurilio Sampaolesi1,2, Silvia Brunelli1,3, Diego Covarello1, Manuela Gavina4, Barbara Rossi6, Gabriela Constantin6, Yvan Torrente4, and Giulio Cossu1,5

1 Stem Cell Research Institute, San Raffaele Hospital, 20132 Milan, Italy
2 Department of Experimental Medicine, Human Anatomy Institute, University of Pavia, 27100 Pavia, Italy
3 Department of Experimental, Environmental Medicine, and Medical Biotechnology, University of Milano-Bicocca, 20126 Milan, Italy
4 Stem Cell Laboratory, Department of Neurological Science, and 5 Department of Biology, University of Milan, 20122 Milan, Italy
6 Department of Pathology, Division of General Pathology, University of Verona, 37129 Verona, Italy

Correspondence to Giulio Cossu: cossu.giulio{at}hsr.it

Efficient delivery of cells to target tissues is a major problem in cell therapy. We report that enhancing delivery of mesoangioblasts leads to a complete reconstitution of downstream skeletal muscles in a mouse model of severe muscular dystrophy ({alpha}-sarcoglycan ko). Mesoangioblasts, vessel-associated stem cells, were exposed to several cytokines, among which stromal- derived factor (SDF) 1 or tumor necrosis factor (TNF) {alpha} were the most potent in enhancing transmigration in vitro and migration into dystrophic muscle in vivo. Transient expression of {alpha}4 integrins or L-selectin also increased several fold migration both in vitro and in vivo. Therefore, combined pretreatment with SDF-1 or TNF-{alpha} and expression of {alpha}4 integrin leads to massive colonization (>50%) followed by reconstitution of >80% of {alpha}-sarcoglycan–expressing fibers, with a fivefold increase in efficiency in comparison with control cells. This study defines the requirements for efficient engraftment of mesoangioblasts and offers a new potent tool to optimize future cell therapy protocols for muscular dystrophies.

Abbreviations used in this paper: ctx, cardiotoxin; HMGB, high mobility group box; ICAM, intercellular adhesion molecule; IL, interleukin; mdx, X chromosome–linked muscular dystrophy; MMP, metalloproteinase; PECAM, platelet endothelial cell adhesion molecule; SDF, stromal-derived factor; SG, sarcoglycan; VCAM, vascular cell adhesion molecule; WT, wild-type.


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