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Free Radic Biol Med. 2018 May 20;120:33-40. doi: 10.1016/j.freeradbiomed.2018.02.024. Epub 2018 Feb 17.

Macrophage-derived superoxide production and antioxidant response following skeletal muscle injury.

Author information

1
Institut NeuroMyoGène, Université Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Lyon, France; Movement Sport and Health Sciences Laboratory, UFR STAPS, Université de Rennes 2, Ecole Normale Supérieure de Rennes, Rennes, France.
2
Institut NeuroMyoGène, Université Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Lyon, France.
3
Ecole Normale Supérieure, Département de Chimie, CNRS UMR 7203, Université Pierre et Marie Curie, Paris, France.
4
Department of Biochemistry and Molecular Biology, Research Center for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
5
Institut NeuroMyoGène, Université Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Lyon, France. Electronic address: remi.mounier@univ-lyon1.fr.

Abstract

Macrophages are key players of immunity that display different functions according to their activation states. In a regenerative context, pro-inflammatory macrophages (Ly6Cpos) are involved in the mounting of the inflammatory response whereas anti-inflammatory macrophages (Ly6Cneg) dampen the inflammation and promote tissue repair. Reactive oxygen species (ROS) production is a hallmark of tissue injury and of subsequent inflammation as described in a bacterial challenge context. However, whether macrophages produce ROS following a sterile tissue injury is uncertain. In this study, we used complementary in vitro, ex vivo and in vivo experiments in mouse to show that macrophages do not release ROS following a sterile injury in skeletal muscle. Furthermore, expression profiles of genes involved in the response to oxidative stress in Ly6Cpos and Ly6Cneg macrophage subsets did not indicate any antioxidant response in this context. Finally, in vivo, pharmacological antioxidant supplementation with N-Acetyl-cysteine (NAC) following skeletal muscle injury did not alter macrophage phenotype during skeletal muscle regeneration. Overall, these results indicate that following a sterile injury, macrophage-derived ROS release is not involved in the regulation of the inflammatory response in the regenerating skeletal muscle.

KEYWORDS:

Oxidative stress; Sterile inflammation; Tissue repair

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