Phagocytosis mediated by scavenger receptor class BI promotes macrophage transition during skeletal muscle regeneration

Zhang, Jing; Qu, Chao; Li, Taotao; Cui, Wei; Wang, Xiaonan; Du, Jie

doi:10.1074/jbc.ra119.008795

Cited by 47 publications

(56 citation statements)

References 48 publications

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“…Therefore, the beneficial effect of RvD1 on muscle regeneration may be attributable to direct positive interactions between intramuscular macrophages and resident myofibers and/or MuSCs. Phagocytosis of muscle cell debris is a key stimulatory cue triggering macrophage polarization (2), and blocking phagocytosis has deleterious effects on both intramuscular macrophage phenotype transitions and myofiber regeneration (3). Therefore, the stimulatory effects of RvD1 on phagocytosis, intramuscular macrophage activity, and myofiber regeneration are likely complex and intrinsically linked.…”

Section: Discussionmentioning

confidence: 99%

“…Muscle length was measured with calipers and optimum fiber length (L f ) determined by multiplying L o by the TA muscle L f /L o ratio of 0.6 (58). The CSA of the muscle was calculated by dividing muscle mass by the product of L f and 1.06 mg/mm 3 (59). sP o was calculated by dividing P o by muscle CSA.…”

Section: Methodsmentioning

confidence: 99%

“…Polymorphonuclear cells (PMNs) appear first within injured muscle, followed by blood monocyte-derived macrophages that invade within necrotic myofibers to engulf and clear tissue debris (2). In addition to preparing the injury site to enable subsequent repair, phagocytosis triggers a switch to a reparative macrophage subset that supports muscle regeneration via interactions with postmitotic muscle cells (myofibers) and associated resident myogenic muscle stem cells (MuSCs) (3). Unlike macrophages, PMNs have overall deleterious effects on muscle regeneration (4).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Resolvin D1 supports skeletal myofiber regeneration via actions on myeloid and muscle stem cells

Markworth¹,

Brown²,

Lim³

et al. 2020

JCI Insight

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Resolvin D1 supports skeletal myofiber regeneration via actions on myeloid and muscle stem cells

Markworth¹,

Brown²,

Lim³

et al. 2020

JCI Insight

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“…Consistent with this hypothesis, RvD1 modulated the MuSC response during muscle regeneration based on an accelerated fusion of proliferated Pax7 + cells and increased expression of the myogenic regulator factor myogenin. Phagocytosis of muscle cell debris is a key stimulatory cue triggering a MΦ polarization (4), and blocking phagocytosis has deleterious effects on both intramuscular MΦ phenotype transitions and myofiber regeneration (6). Therefore, the stimulatory effects of RvD1 on phagocytosis, intramuscular MΦ activity, and myofiber regeneration are likely to be complex and intrinsically linked.…”

Section: Discussionmentioning

confidence: 99%

Immunoresolvents Support Skeletal Myofiber Regeneration via Actions on Myeloid and Muscle Stem Cells

Markworth

Brown

Lim

et al. 2020

Preprint

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150-word limit):Specialized pro-resolving mediators (SPMs) actively limit inflammation and expedite its resolution. Here we profiled intramuscular lipid mediators following injury and investigated the role of SPMs in skeletal muscle inflammation and repair. Both eicosanoids and SPMs increased following myofiber damage induced by intramuscular injection of barium chloride or functional overload. Daily systemic administration of resolvin D1 (RvD1) limited the degree and duration of inflammation, enhanced regenerating myofiber growth, and improved recovery of muscle strength. RvD1 suppressed inflammatory cytokines, enhanced polymorphonuclear cell clearance, modulated muscle stem cells, and polarized macrophages to a more pro-regenerative subset. RvD1 had minimal direct impact on in-vitro myogenesis but directly suppressed myokine production and stimulated macrophage phagocytosis, showing that SPMs influence modulate both infiltrating myeloid and resident muscle cells. These data reveal the efficacy of immunoresolvents as a novel alternative to classical anti-inflammatory interventions in the management of muscle injuries to modulate inflammation while stimulating tissue repair.3 Introduction:

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“…GC/GR signaling enhances the efferocytic properties of macrophages (Giles et al, 2001;Heasman et al, 2003;Stolberg et al, 2015), for instance, by increasing the expression of Mertk or Anxa1 as a core aspect of their anti-inflammatory effects (Koenen et al, 2018;Yona and Gordon, 2007;Zizzo et al, 2012). Efferocytosis is associated with macrophage polarization state since it induces the acquisition of an anti-inflammatory/resolving phenotype (Fadok et al, 1998;Han et al, 2016;Huynh et al, 2002;Zhang et al, 2019a), thus provides a bridge in macrophage function across sterile and LPS induced inflammation. In that context, our results show that genes downregulated in AMPK-deficient macrophages upon GC treatment were associated with autophagy and/or phagocytic processes.…”

Section: Discussionmentioning

confidence: 99%

AMPKα1 is essential for Glucocorticoid Receptor triggered anti-inflammatory macrophage activation

Caratti¹,

Desgeorges

Juban

et al. 2020

Preprint

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words)Macrophages are key immune cells in mediating both the acute inflammatory phase and the repair phase after tissue damage. Macrophages switch from pro-inflammatory to antiinflammatory cells that sustain tissue repair and return to homeostasis. We show that the metabolic sensor, AMP-activated protein kinase (AMPK) is essential for glucocorticoid induction of an anti-inflammatory macrophage phenotype. While canonical gene regulation by glucocorticoids was not affected by loss of AMPK, we identified glucocorticoid-regulated genes in macrophages, which are dependent on AMPK expression and related to efferocytosis. AMPK-deficient macrophages do not acquire the phenotypic and functional antiinflammatory features upon glucocorticoid exposure. Loss of AMPK in macrophages in vivo abrogates glucocorticoid anti-inflammatory actions in both sterile muscle damage and endotoxin induced acute lung injury. These data highlight that the glucocorticoid receptor is dependent on AMPK for its immune modulatory actions in macrophages, linking their metabolic status to transcriptional control in operating the resolution of inflammation.

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Phagocytosis mediated by scavenger receptor class BI promotes macrophage transition during skeletal muscle regeneration

Cited by 47 publications

References 48 publications

Resolvin D1 supports skeletal myofiber regeneration via actions on myeloid and muscle stem cells

Resolvin D1 supports skeletal myofiber regeneration via actions on myeloid and muscle stem cells

Immunoresolvents Support Skeletal Myofiber Regeneration via Actions on Myeloid and Muscle Stem Cells

AMPKα1 is essential for Glucocorticoid Receptor triggered anti-inflammatory macrophage activation

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