The Role of Carbon-Carbon Chemokine Receptor 1 in Skeletal Muscle Regeneration

Diaphragmatic myotubes are known to constitutively express CCR1, a chemokine receptor in the C-C chemokine family, when cultured in vitro. It has been shown that CCR1 and its ligand CCL3 (MIP-1a) are directly involved in muscle repair responses in vitro. Furthermore, in vivo experiments, carried out in the MDX mouse model of muscular dystrophy, showed that these molecules were up-regulated in the dystrophic diaphragm muscle thus suggesting a role for CCR1 in inflammation and muscle healing. In this study, indeed, the role of CCR1 was investigated, with focus on inflammatory cell infiltration within the injured muscle using the freeze injury murine model. This study suggested that there is no significant difference in muscle regeneration or infiltration between CCR1-/- mice and their wild-type controls. There was also no difference in the muscle force between the knockout and their controls at 3, 7, and 14 days post injury. Investigation of individual infiltrating cell (macrophage, CD4 T-cells, CD8 T-cells) populations in the injured tissue yielded no significant difference. These data suggest that, although CCR1 has been found to play a role in myoblast proliferation and migration in vitro, it does not seem to have any apparent effect on muscle regeneration in vivo in the context of the freeze-injury model.