Résumé :
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Galectins belong to a family of soluble proteins that can be found both extracellularly and intracellularly. In vivo, their localisation is highly regulated depending on physiological situations. Several studies has established that, in addition to their lectinic property (i.e. binding to specific carbohydrates), galectins can also be involved in protein-protein interactions. To elucidate the role of galectins in vivo, we have undertaken a genetic analysis of several of them. Galectin1 is express into the mesoderm, specially in muscles. Galectin 1-/- mice have been created in the laboratory and they are viable and fertile, and don't display any overt phenotype in the protective environment of the animal house. Our finding that adult galectin 1-/- mice have a reduced capacity to repair muscle injury induced after cardiotoxin injection (1) laid us to examine their stem cells. We then discovered that galectin 1 is expressed in these cells and made the hypothese that the lack of Galectin1 in the mutant mice may affect them and partially account for the defect in muscle regeneration. We have quantitatively and qualitatively compared satellite cells from control (wt) and mutant (galectin 1-/-) animals using isolated muscle fibers from adult animals. The results show that the absolute number of satellite cells is not affected by the absence of galectin 1. But we found that the in vitro activation capacity of mutant satellite cells is drastically impaired. Indeed, the total number of daughter cells generated after 3 days of serum stimulation is 5-fold lower for mutant satellite cells than for wt satellite cells. The properties of cells generated by wt and mutant satellite cells are now been compared in order to pinpoint the nature of the defect(s) induced by the absence of galectin 1. Better understanding the role(s) of galectin 1 in the repair of muscle injury may ultimately contribute to improved therapy for muscle-related diseases.
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