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Stem Cells International
Volume 2012, Article ID 412610, 7 pages
http://dx.doi.org/10.1155/2012/412610
Research Article

Human Muscle Progenitor Cells Displayed Immunosuppressive Effect through Galectin-1 and Semaphorin-3A

1INSERM UMR940, Institut Universitaire d'Hématologie, 75475 Paris Cedex 10, France
2Unité de Thérapie Cellulaire et CIC de Biothérapies, Hôpital Saint Louis, AP-HP, 75475 Paris Cedex 10, France
3Université Paris Diderot, Sorbonne Paris Cité, 75475 Paris, France
4CNRS UMR 8147, Hôpital Necker and Université Paris Descartes, 75743 Paris Cedex 15, France
5Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, CNRS UMR 8601, Université Paris Descartes, 75006 Paris, France
6TRAGEX PHARMA, 75015 Paris, France
7Service d'Hématologie Clinique, Hôpital d'Amiens, 80054 Amiens Cedex 1, France

Received 3 January 2012; Revised 27 February 2012; Accepted 27 February 2012

Academic Editor: J. Gimble

Copyright © 2012 Séverine Lecourt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In human skeletal muscle, myoblasts represent the main population of myogenic progenitors. We previously showed that, beside their myogenic differentiation capacities, myoblasts also differentiate towards osteogenic and chondrogenic lineages, some properties generally considered being hallmarks of mesenchymal stem cells (MSCs). MSCs are also characterized by their immunosuppressive potential, through cell-cell contacts and soluble factors, including prostaglandin E-2 (PGE-2), transforming growth factor-β1 (TGF-β1), interleukine-10, or indoleamine 2,3-dioxygenase. We and others also reported that Galectin-1 (Gal-1) and Semaphorin-3A (Sema-3A) were involved in MSCs-mediated immunosuppression. Here, we show that human myoblasts induce a significant and dose-dependant proliferation inhibition, independently of PGE-2 and TGF-β1. Our experiments revealed that myoblasts, in culture or in situ in human muscles, expressed and secreted Gal-1 and Sema-3A. Furthermore, myoblasts immunosuppressive functions were reverted by using blocking antibodies against Gal-1 or Sema-3A. Together, these results demonstrate an unsuspected immunosuppressive effect of myoblasts that may open new therapeutic perspectives.