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

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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
    CNRS, UMR8104
    University of Paris Descartes, Sorbonne Paris Cite)

  • 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
    CNRS, UMR8104
    University of Paris Descartes, Sorbonne Paris Cite)

  • Bénédicte Chazaud

    (Inserm, U1016, Institut Cochin
    CNRS, UMR8104
    University of Paris Descartes, Sorbonne Paris Cite)

  • 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))

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.

Suggested Citation

  • Ludovic Arnold & Hélène Perrin & Camille Baudesson de Chanville & Marielle Saclier & Patricia Hermand & Lucie Poupel & Elodie Guyon & Fabrice Licata & Wassila Carpentier & José Vilar & Rémi Mounier & , 2015. "CX3CR1 deficiency promotes muscle repair and regeneration by enhancing macrophage ApoE production," Nature Communications, Nature, vol. 6(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9972
    DOI: 10.1038/ncomms9972
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