AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration. / Mounier, Rémi; Théret, Marine; Arnold, Ludovic; Cuvellier, Sylvain; Bultot, Laurent; Göransson, Olga; Sanz, Nieves; Ferry, Arnaud; Sakamoto, Kei; Foretz, Marc; Viollet, Benoit; Chazaud, Bénédicte.

In: Cell Metabolism, Vol. 18, No. 2, 06.08.2013, p. 251-264.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Mounier, R, Théret, M, Arnold, L, Cuvellier, S, Bultot, L, Göransson, O, Sanz, N, Ferry, A, Sakamoto, K, Foretz, M, Viollet, B & Chazaud, B 2013, 'AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration', Cell Metabolism, vol. 18, no. 2, pp. 251-264. https://doi.org/10.1016/j.cmet.2013.06.017

APA

Mounier, R., Théret, M., Arnold, L., Cuvellier, S., Bultot, L., Göransson, O., Sanz, N., Ferry, A., Sakamoto, K., Foretz, M., Viollet, B., & Chazaud, B. (2013). AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration. Cell Metabolism, 18(2), 251-264. https://doi.org/10.1016/j.cmet.2013.06.017

Vancouver

Mounier R, Théret M, Arnold L, Cuvellier S, Bultot L, Göransson O et al. AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration. Cell Metabolism. 2013 Aug 6;18(2):251-264. https://doi.org/10.1016/j.cmet.2013.06.017

Author

Mounier, Rémi ; Théret, Marine ; Arnold, Ludovic ; Cuvellier, Sylvain ; Bultot, Laurent ; Göransson, Olga ; Sanz, Nieves ; Ferry, Arnaud ; Sakamoto, Kei ; Foretz, Marc ; Viollet, Benoit ; Chazaud, Bénédicte. / AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration. In: Cell Metabolism. 2013 ; Vol. 18, No. 2. pp. 251-264.

Bibtex

@article{e956c287f2904fb787d0a524b99327ef,
title = "AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration",
abstract = "Macrophages control the resolution of inflammation through the transition from a proinflammatory (M1) to an anti-inflammatory (M2) phenotype. Here, we present evidence for a role of AMPKα1, a master regulator of energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired in AMPKα1-/- mice. In vivo loss-of-function (LysM-Cre;AMPKα1fl/fl mouse) and rescue (bone marrow transplantation) experiments showed that macrophagic AMPKα1 was required for muscle regeneration. Cell-based experiments revealed that AMPKα1-/- macrophages did not fully acquire the phenotype or the functions of M2 cells. In vivo, AMPKα1-/- leukocytes did not acquire the expression of M2 markers during muscle regeneration. Skewing from M1 toward M2 phenotype upon phagocytosis of necrotic and apoptotic cells was impaired in AMPKα1-/- macrophages and when AMPK activation was prevented by the inhibition of its upstream activator, CaMKKβ. In conclusion, AMPKα1 is crucial for phagocytosis-induced macrophage skewing from a pro- to anti-inflammatory phenotype at the time of resolution of inflammation.",
author = "R{\'e}mi Mounier and Marine Th{\'e}ret and Ludovic Arnold and Sylvain Cuvellier and Laurent Bultot and Olga G{\"o}ransson and Nieves Sanz and Arnaud Ferry and Kei Sakamoto and Marc Foretz and Benoit Viollet and B{\'e}n{\'e}dicte Chazaud",
year = "2013",
month = aug,
day = "6",
doi = "10.1016/j.cmet.2013.06.017",
language = "English",
volume = "18",
pages = "251--264",
journal = "Cell Metabolism",
issn = "1550-4131",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - AMPKα1 regulates macrophage skewing at the time of resolution of inflammation during skeletal muscle regeneration

AU - Mounier, Rémi

AU - Théret, Marine

AU - Arnold, Ludovic

AU - Cuvellier, Sylvain

AU - Bultot, Laurent

AU - Göransson, Olga

AU - Sanz, Nieves

AU - Ferry, Arnaud

AU - Sakamoto, Kei

AU - Foretz, Marc

AU - Viollet, Benoit

AU - Chazaud, Bénédicte

PY - 2013/8/6

Y1 - 2013/8/6

N2 - Macrophages control the resolution of inflammation through the transition from a proinflammatory (M1) to an anti-inflammatory (M2) phenotype. Here, we present evidence for a role of AMPKα1, a master regulator of energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired in AMPKα1-/- mice. In vivo loss-of-function (LysM-Cre;AMPKα1fl/fl mouse) and rescue (bone marrow transplantation) experiments showed that macrophagic AMPKα1 was required for muscle regeneration. Cell-based experiments revealed that AMPKα1-/- macrophages did not fully acquire the phenotype or the functions of M2 cells. In vivo, AMPKα1-/- leukocytes did not acquire the expression of M2 markers during muscle regeneration. Skewing from M1 toward M2 phenotype upon phagocytosis of necrotic and apoptotic cells was impaired in AMPKα1-/- macrophages and when AMPK activation was prevented by the inhibition of its upstream activator, CaMKKβ. In conclusion, AMPKα1 is crucial for phagocytosis-induced macrophage skewing from a pro- to anti-inflammatory phenotype at the time of resolution of inflammation.

AB - Macrophages control the resolution of inflammation through the transition from a proinflammatory (M1) to an anti-inflammatory (M2) phenotype. Here, we present evidence for a role of AMPKα1, a master regulator of energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired in AMPKα1-/- mice. In vivo loss-of-function (LysM-Cre;AMPKα1fl/fl mouse) and rescue (bone marrow transplantation) experiments showed that macrophagic AMPKα1 was required for muscle regeneration. Cell-based experiments revealed that AMPKα1-/- macrophages did not fully acquire the phenotype or the functions of M2 cells. In vivo, AMPKα1-/- leukocytes did not acquire the expression of M2 markers during muscle regeneration. Skewing from M1 toward M2 phenotype upon phagocytosis of necrotic and apoptotic cells was impaired in AMPKα1-/- macrophages and when AMPK activation was prevented by the inhibition of its upstream activator, CaMKKβ. In conclusion, AMPKα1 is crucial for phagocytosis-induced macrophage skewing from a pro- to anti-inflammatory phenotype at the time of resolution of inflammation.

UR - http://www.scopus.com/inward/record.url?scp=84881356321&partnerID=8YFLogxK

U2 - 10.1016/j.cmet.2013.06.017

DO - 10.1016/j.cmet.2013.06.017

M3 - Journal article

C2 - 23931756

AN - SCOPUS:84881356321

VL - 18

SP - 251

EP - 264

JO - Cell Metabolism

JF - Cell Metabolism

SN - 1550-4131

IS - 2

ER -

ID: 239216529