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AMPK alpha 1 Regulates Macrophage Skewing at the Time of Resolution of Inflammation during Skeletal Muscle Regeneration

Mounier, Remi ; Theret, Marine ; Arnold, Ludovic ; Cuvellier, Sylvain ; Bultot, Laurent ; Göransson, Olga LU orcid ; Sanz, Nieves ; Ferry, Arnaud ; Sakamoto, Kei and Foretz, Marc , et al. (2013) In Cell Metabolism 18(2). p.251-264
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 AMPK alpha 1, a master regulator of energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired in AMPK alpha 1(-/-) mice. In vivo loss-of-function (LysM-Cre;AMPK alpha 1(fl/fl) mouse) and rescue (bone marrow transplantation) experiments showed that macrophagic AMPK alpha 1 was required for muscle regeneration. Cell-based experiments revealed that AMPK alpha 1(-/-) macrophages did not fully acquire the phenotype or the functions of M2 cells. In vivo, AMPK alpha 1(-/-) leukocytes did not acquire the... (More)
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 AMPK alpha 1, a master regulator of energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired in AMPK alpha 1(-/-) mice. In vivo loss-of-function (LysM-Cre;AMPK alpha 1(fl/fl) mouse) and rescue (bone marrow transplantation) experiments showed that macrophagic AMPK alpha 1 was required for muscle regeneration. Cell-based experiments revealed that AMPK alpha 1(-/-) macrophages did not fully acquire the phenotype or the functions of M2 cells. In vivo, AMPK alpha 1(-/-) 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 AMPK alpha 1(-/-) macrophages and when AMPK activation was prevented by the inhibition of its upstream activator, CaMKK beta. In conclusion, AMPK alpha 1 is crucial for phagocytosis-induced macrophage skewing from a pro-to anti-inflammatory phenotype at the time of resolution of inflammation. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cell Metabolism
volume
18
issue
2
pages
251 - 264
publisher
Cell Press
external identifiers
  • wos:000326267200012
  • scopus:84881356321
ISSN
1550-4131
DOI
10.1016/j.cmet.2013.06.017
language
English
LU publication?
yes
id
8ae0433f-c7c1-4f5f-8f14-ac906b72b6c9 (old id 4204093)
date added to LUP
2016-04-01 10:09:03
date last changed
2024-04-07 02:01:26
@article{8ae0433f-c7c1-4f5f-8f14-ac906b72b6c9,
  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 AMPK alpha 1, a master regulator of energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired in AMPK alpha 1(-/-) mice. In vivo loss-of-function (LysM-Cre;AMPK alpha 1(fl/fl) mouse) and rescue (bone marrow transplantation) experiments showed that macrophagic AMPK alpha 1 was required for muscle regeneration. Cell-based experiments revealed that AMPK alpha 1(-/-) macrophages did not fully acquire the phenotype or the functions of M2 cells. In vivo, AMPK alpha 1(-/-) 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 AMPK alpha 1(-/-) macrophages and when AMPK activation was prevented by the inhibition of its upstream activator, CaMKK beta. In conclusion, AMPK alpha 1 is crucial for phagocytosis-induced macrophage skewing from a pro-to anti-inflammatory phenotype at the time of resolution of inflammation.}},
  author       = {{Mounier, Remi and Theret, Marine and Arnold, Ludovic and Cuvellier, Sylvain and Bultot, Laurent and Göransson, Olga and Sanz, Nieves and Ferry, Arnaud and Sakamoto, Kei and Foretz, Marc and Viollet, Benoit and Chazaud, Benedicte}},
  issn         = {{1550-4131}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{251--264}},
  publisher    = {{Cell Press}},
  series       = {{Cell Metabolism}},
  title        = {{AMPK alpha 1 Regulates Macrophage Skewing at the Time of Resolution of Inflammation during Skeletal Muscle Regeneration}},
  url          = {{http://dx.doi.org/10.1016/j.cmet.2013.06.017}},
  doi          = {{10.1016/j.cmet.2013.06.017}},
  volume       = {{18}},
  year         = {{2013}},
}