Abstract:
:Muscle injury triggers inflammation in which infiltrating mononuclear phagocytes are crucial for tissue regeneration. The interaction of the CCL2/CCR2 and CX3CL1/CX3CR1 chemokine axis that guides phagocyte infiltration is incompletely understood. Here, we show that CX3CR1 deficiency promotes muscle repair and rescues Ccl2(-/-) mice from impaired muscle regeneration as a result of altered macrophage function, not infiltration. Transcriptomic analysis of muscle mononuclear phagocytes reveals that Apolipoprotein E (ApoE) is upregulated in mice with efficient regeneration. ApoE treatment enhances phagocytosis by mononuclear phagocytes in vitro, and restores phagocytic activity and muscle regeneration in Ccl2(-/-) mice. Because CX3CR1 deficiency may compensate for defective CCL2-dependant monocyte recruitment by modulating ApoE-dependent macrophage phagocytic activity, targeting CX3CR1 expressed by macrophages might be a powerful therapeutic approach to improve muscle regeneration.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Arnold L,Perrin H,de Chanville CB,Saclier M,Hermand P,Poupel L,Guyon E,Licata F,Carpentier W,Vilar J,Mounier R,Chazaud B,Benhabiles N,Boissonnas A,Combadiere B,Combadiere Cdoi
10.1038/ncomms9972subject
Has Abstractpub_date
2015-12-03 00:00:00pages
8972issn
2041-1723pii
ncomms9972journal_volume
6pub_type
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