Anti-inflammatory macrophages improve skeletal muscle recovery from ischemia-reperfusion

Hammers, David W.; Rybalko, Viktoriya; Merscham-Banda, Melissa; Hsieh, Pei‐Ling; Suggs, Laura J.; Farrar, Roger P.

doi:10.1152/japplphysiol.00313.2014

Cited by 39 publications

(42 citation statements)

References 51 publications

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“…Increased collagen deposition in PEG-Fib and PEG-Fib/SDF-1α treated muscles may be indicative of M2 macrophage activity in the inflammatory setting. 70 These cells appear in the muscles as early as 3 days post-reperfusion 71 and produce arginase-1 and TGF-β factors both of which contribute to extra-cellular matrix deposition. 72 Overall, there appears to be no functional benefit from SDF-1α treatment up to 14 days post-TK-I/R injury compared to matrix delivery alone, despite apparent enhancement in neovascularization.…”

Section: Discussionmentioning

confidence: 99%

Controlled delivery of SDF-1α and IGF-1: CXCR4⁺ cell recruitment and functional skeletal muscle recovery

et al. 2015

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Therapeutic delivery of regeneration-promoting biological factors directly to the site of injury has demonstrated its efficacy in various injury models. Several reports describe improved tissue regeneration following local injection of tissue specific growth factors, cytokines and chemokines. Evidence exists that combined cytokine/growth factor treatment is superior for optimizing tissue repair by targeting different aspects of the regeneration response. The purpose of this study was to evaluate the therapeutic potential of the controlled delivery of stromal cell-derived factor-1alpha (SDF-1α) alone or in combination with insulin-like growth factor-I (SDF-1α/IGF-I) for the treatment of tourniquet-induced ischemia/reperfusion injury (TK-I/R) of skeletal muscle. We hypothesized that SDF-1α will promote sustained stem cell recruitment to the site of muscle injury, while IGF-I will induce progenitor cell differentiation to effectively restore muscle contractile function after TK-I/R injury while concurrently reducing apoptosis. Utilizing a novel poly-ethylene glycol PEGylated fibrin gel matrix (PEG-Fib), we incorporated SDF-1α alone (PEG-Fib/SDF-1α) or in combination with IGF-I (PEG-Fib/SDF-1α/IGF-I) for controlled release at the site of acute muscle injury. Despite enhanced cell recruitment and revascularization of the regenerating muscle after SDF-1α treatment, functional analysis showed no benefit from PEG-Fib/SDF-1α therapy, while dual delivery of PEG-Fib/SDF-1α/IGF-I resulted in IGF-I-mediated improvement of maximal force recovery and SDF-1α-driven in vivo neovasculogenesis. Histological data supported functional data, as well as highlighted the important differences in the regeneration process among treatment groups. This study provides evidence that while revascularization may be necessary for maximizing muscle force recovery, without modulation of other effects of inflammation it is insufficient.

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Section: Discussionmentioning

confidence: 99%

Controlled delivery of SDF-1α and IGF-1: CXCR4⁺ cell recruitment and functional skeletal muscle recovery

et al. 2015

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“…In skeletal muscle, there are 2 distinct subtypes of macrophages that can be distinguished by their surface marker expression. The F4/80 and CD11b markers are expressed by all macrophages, whereas Ly‐6C is highly expressed by the inflammatory macrophage subtype . In contrast, the anti‐inflammatory macrophage subtype expressed low levels of Ly‐6C and high levels of F4/80 .…”

Section: Methodsmentioning

confidence: 98%

Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

2018

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“…activity (124,171) and contribute to the no-reflow phenomenon (62,63), increasing I/R-induced tissue damage. Macrophages reach the ischemic site 48 -72 h after reperfusion (68,170). Their exact role remains unclear, since they may be implicated in both I/R-induced tissue damage and recovery; Hammers et al (68) identified two prominent macrophage populations (inflammatory and anti-inflammatory) at 3 and 5 days of reperfusion.…”

Section: Phenomena Associated With Skeletal Muscle Injuries Followingmentioning

confidence: 99%

“…Macrophages reach the ischemic site 48 -72 h after reperfusion (68,170). Their exact role remains unclear, since they may be implicated in both I/R-induced tissue damage and recovery; Hammers et al (68) identified two prominent macrophage populations (inflammatory and anti-inflammatory) at 3 and 5 days of reperfusion. Noncellular factors, especially natural IgM, also mediate reperfusion injury by recognizing nonmuscle myosin heavy chain type II expressed during ischemia and activating the complement system (6,201).…”

Section: Phenomena Associated With Skeletal Muscle Injuries Followingmentioning

confidence: 99%

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

Paradis

Charles

Meyer

et al. 2016

American Journal of Physiology-Cell Physiology

100

127

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Peripheral artery disease (PAD) is a common circulatory disorder of the lower limb arteries that reduces functional capacity and quality of life of patients. Despite relatively effective available treatments, PAD is a serious public health issue associated with significant morbidity and mortality. Ischemia-reperfusion (I/R) cycles during PAD are responsible for insufficient oxygen supply, mitochondriopathy, free radical production, and inflammation and lead to events that contribute to myocyte death and remote organ failure. However, the chronology of mitochondrial and cellular events during the ischemic period and at the moment of reperfusion in skeletal muscle fibers has been poorly reviewed. Thus, after a review of the basal myocyte state and normal mitochondrial biology, we discuss the physiopathology of ischemia and reperfusion at the mitochondrial and cellular levels. First we describe the chronology of the deleterious biochemical and mitochondrial mechanisms activated by I/R. Then we discuss skeletal muscle I/R injury in the muscle environment, mitochondrial dynamics, and inflammation. A better understanding of the chronology of the events underlying I/R will allow us to identify key factors in the development of this pathology and point to suitable new therapies. Emerging data on mitochondrial dynamics should help identify new molecular and therapeutic targets and develop protective strategies against PAD.peripheral artery disease; ischemia-reperfusion; skeletal muscle; mitochondria; oxidative stress PERIPHERAL ARTERY DISEASE (PAD) refers to a common circulatory disorder of the lower limb caused by chronic narrowing of the arteries (e.g., stenosis and occlusion) or atherosclerosis. PAD represents a broad spectrum of disease severity, ranging from asymptomatic disease to frequent pain when walking (i.e., intermittent claudication or limping) or critical limb ischemia associated with decubitus pain and/or ulcers (114,126).PAD is known to be associated with reduced functional capacity and quality of life. It is a major cause of limb amputation, as well as an increased risk factor for myocardial infarction, stroke, and death. The incidence of PAD varies with age, from 3-10% in young people to 15-20% in people Ͼ70 yr of age, and is asymptomatic in 40% of the cases (1), with greater prevalence among men. The major PAD risk factors, including smoking, diabetes mellitus, dyslipidemia, hypertension, and obesity, are the same as those for cardiovascular and cerebrovascular diseases (35).Three main complementary treatment options improve the functional status and other clinical outcomes in PAD patients (54). 1) Optimization of medical therapy (i.e., pharmacotherapy) reduces the risk of cardiac ischemia, increases the distance a patient can walk, and improves the functional capacity of patients. 2) When possible, exercise training, a noninvasive and nonpharmacological therapy, improves walking ability and has protective effects in patients with PAD characterized by intermittent claudication and infrainguinal lesions...

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Anti-inflammatory macrophages improve skeletal muscle recovery from ischemia-reperfusion

Cited by 39 publications

References 51 publications

Controlled delivery of SDF-1α and IGF-1: CXCR4⁺ cell recruitment and functional skeletal muscle recovery

Controlled delivery of SDF-1α and IGF-1: CXCR4⁺ cell recruitment and functional skeletal muscle recovery

Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

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Anti-inflammatory macrophages improve skeletal muscle recovery from ischemia-reperfusion

Cited by 39 publications

References 51 publications

Controlled delivery of SDF-1α and IGF-1: CXCR4+ cell recruitment and functional skeletal muscle recovery

Controlled delivery of SDF-1α and IGF-1: CXCR4+ cell recruitment and functional skeletal muscle recovery

Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

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Controlled delivery of SDF-1α and IGF-1: CXCR4⁺ cell recruitment and functional skeletal muscle recovery

Controlled delivery of SDF-1α and IGF-1: CXCR4⁺ cell recruitment and functional skeletal muscle recovery