CX3CR1 deficiency promotes muscle repair and regeneration by enhancing macrophage ApoE production

Ludovic Arnold, Hélène Perrin, Camille Baudesson de Chanville, Marielle Saclier, Patricia Hermand, Lucie Poupel, Elodie Guyon, Fabrice Licata, Wassila Carpentier, José Vilar, Rémi Mounier, Bénédicte Chazaud, Nora Benhabiles, Alexandre Boissonnas, Béhazine Combadiere and Christophe Combadiere ()
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Ludovic Arnold: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Hélène Perrin: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Camille Baudesson de Chanville: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Marielle Saclier: Inserm, U1016, Institut Cochin
Patricia Hermand: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Lucie Poupel: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Elodie Guyon: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Fabrice Licata: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Wassila Carpentier: Sorbonne Universités, UPMC Univ Paris 06, Plateforme Post-Génomique de la Pitié-Salpêtrière (P3S), UMS2 Omique, INSERM US029
José Vilar: Paris Centre de Recherche Cardiovasculaire (PARCC) – HEGP
Rémi Mounier: Inserm, U1016, Institut Cochin
Bénédicte Chazaud: Inserm, U1016, Institut Cochin
Nora Benhabiles: CEA, List institute CEA Saclay, Digitéo Labs, PC192
Alexandre Boissonnas: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Béhazine Combadiere: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)
Christophe Combadiere: Sorbonne Universités, UPMC Univ Paris 06, Inserm, U1135, CNRS, ERL 8255, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris)

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms9972

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