Meteorin-like facilitates skeletal muscle repair through a Stat3/IGF-1 mechanism

被引:141
作者
Baht, Gurpreet S. [1 ,2 ]
Bareja, Akshay [1 ,3 ]
Lee, David E. [1 ,3 ]
Rao, Rajesh R. [4 ]
Huang, Rong [1 ,2 ]
Huebner, Janet L. [1 ]
Bartlett, David B. [1 ,5 ,6 ]
Hart, Cory R. [7 ]
Gibson, Jason R. [1 ]
Lanza, Ian R. [7 ]
Kraus, Virginia B. [1 ,3 ,5 ]
Gregory, Simon G. [1 ,8 ]
Spiegelman, Bruce M. [9 ]
White, James P. [1 ,3 ,5 ]
机构
[1] Duke Univ, Sch Med, Duke Mol Physiol Inst, Durham, NC 27708 USA
[2] Duke Univ, Sch Med, Dept Orthopaed Surg, Durham, NC 27708 USA
[3] Duke Univ, Sch Med, Dept Med, Durham, NC 27706 USA
[4] Novartis Res Fdn, Genom Inst, San Diego, CA USA
[5] Duke Univ, Sch Med, Duke Ctr Study Aging & Human Dev, Durham, NC 27708 USA
[6] Duke Univ, Dept Med, Div Med Oncol, Durham, NC USA
[7] Mayo Clin, Coll Med, Div Endocrinol & Metab, Rochester, MN USA
[8] Duke Univ, Sch Med, Dept Neurol, Durham, NC USA
[9] Harvard Med Sch, Dana Farber Canc Inst, Dept Cell Biol, Boston, MA 02115 USA
关键词
GROWTH-FACTOR-I; MACROPHAGES; STAT3; EXPRESSION; DIFFERENTIATION; INTERLEUKIN-6; REGENERATION; ACTIVATION; IL-10;
D O I
10.1038/s42255-020-0184-y
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The immune system plays a multifunctional role throughout the regenerative process, regulating both pro-/anti-inflammatory phases and progenitor cell function. In the present study, we identify the myokine/cytokine Meteorin-like (Metrnl) as a critical regulator of muscle regeneration. Mice genetically lacking Metrnl have impaired muscle regeneration associated with a reduction in immune cell infiltration and an inability to transition towards an anti-inflammatory phenotype. Isochronic parabiosis, joining wild-type and whole-body Metrnl knock-out (KO) mice, returns Metrnl expression in the injured muscle and improves muscle repair, providing supportive evidence for Metrnl secretion from infiltrating immune cells. Macrophage-specific Metrnl KO mice are also deficient in muscle repair. During muscle regeneration, Metrnl works, in part, through Stat3 activation in macrophages, resulting in differentiation to an anti-inflammatory phenotype. With regard to myogenesis, Metrnl induces macrophage-dependent insulin-like growth factor 1 production, which has a direct effect on primary muscle satellite cell proliferation. Perturbations in this pathway inhibit efficacy of Metrnl in the regenerative process. Together, these studies identify Metrnl as an important regulator of muscle regeneration and a potential therapeutic target to enhance tissue repair.
引用
收藏
页码:278 / +
页数:24
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