作者: Rémi Mounier , Marine Théret , Ludovic Arnold , Sylvain Cuvellier , Laurent Bultot
DOI: 10.1016/J.CMET.2013.06.017
关键词:
摘要: Macrophages control the resolution of inflammation through transition from a proinflammatory (M1) to an anti-inflammatory (M2) phenotype. Here, we present evidence for role AMPKα1, master regulator energy homeostasis, in macrophage skewing that occurs during skeletal muscle regeneration. Muscle regeneration was impaired AMPKα1(-/-) mice. In vivo loss-of-function (LysM-Cre;AMPKα1(fl/fl) mouse) and rescue (bone marrow transplantation) experiments showed macrophagic AMPKα1 required Cell-based revealed macrophages did not fully acquire phenotype or functions M2 cells. In vivo, leukocytes expression markers Skewing M1 toward upon phagocytosis necrotic apoptotic cells when AMPK activation prevented by inhibition its upstream activator, CaMKKβ. In conclusion, is crucial phagocytosis-induced pro- at time inflammation.