The skeletal muscle regeneration occurs due to the presence of tissue specific stem cells - satellite
cells. These cells, localized between sarcolemma and basal lamina, are bound to muscle fibers and
remain quiescent until their activation upon muscle injury. Due to pathological conditions, such as
extensive injury or dystrophy, skeletal muscle regeneration is diminished. Among the therapies
aiming to ameliorate skeletal muscle diseases are transplantations of the stem cells. In our previous
studies we showed that Sdf-1 (stromal derived factor ¡1) increased migration of stem cells and
their fusion with myoblasts in vitro. Importantly, we identified that Sdf-1 caused an increase in the
expression of tetraspanin CD9 - adhesion protein involved in myoblasts fusion. In the current study
we aimed to uncover the details of molecular mechanism of Sdf-1 action. We focused at the Sdf-1
receptors - Cxcr4 and Cxcr7, as well as signaling pathways induced by these molecules in primary
myoblasts, as well as various stem cells - mesenchymal stem cells and embryonic stem cells, i.e. the
cells of different migration and myogenic potential. We showed that Sdf-1 altered actin
organization via FAK (focal adhesion kinase), Cdc42 (cell division control protein 42), and Rac-1 (Ras-
Related C3 Botulinum Toxin Substrate 1). Moreover, we showed that Sdf-1 modified the
transcription profile of genes encoding factors engaged in cells adhesion and migration. As the
result, cells such as primary myoblasts or embryonic stem cells, became characterized by more
effective migration when transplanted into regenerating muscle
