Physiological role of tumor necrosis factor α in traumatic muscle injury

Warren, Gordon L.; Hulderman, Tracy; Jensen, Nancy J.; McKinstry, Michael; Mishra, Michael; Luster, Michael I.; Simeonova, Petia P.

doi:10.1096/fj.02-0187fje

Cited by 226 publications

(227 citation statements)

References 39 publications

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“…Following muscle injury, the early invading neutrophil and macrophage populations express TNF-␣ (15,137), suggesting that the cytokine may contribute to the early inflammatory stages that precede muscle regeneration. TNF-␣ levels in muscle following acute injury peak at 24 h postinjury, which indicates that TNF-␣ production is most tightly coupled with the Th1 inflammatory response in injured muscle (126). Because findings show that TNF-␣ induces iNOS in myeloid cells and that myeloid cell-derived NO can cause muscle fiber damage that occurs during the early, Th1 inflammatory response following muscle injury, TNF-␣ activation of inflammatory cells has been associated with promoting muscle damage.…”

Section: Do Neutrophil-derived or M1 Macrophage-derived Molecules Modmentioning

confidence: 77%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

907

987

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Tidball JG, Villalta SA. Regulatory interactions between muscle and the immune system during muscle regeneration. Am J Physiol Regul Integr Comp Physiol 298: R1173-R1187, 2010. First published March 10, 2010 doi:10.1152/ajpregu.00735.2009.-Recent discoveries reveal complex interactions between skeletal muscle and the immune system that regulate muscle regeneration. In this review, we evaluate evidence that indicates that the response of myeloid cells to muscle injury promotes muscle regeneration and growth. Acute perturbations of muscle activate a sequence of interactions between muscle and inflammatory cells. The initial inflammatory response is a characteristic Th1 inflammatory response, first dominated by neutrophils and subsequently by CD68 ϩ M1 macrophages. M1 macrophages can propagate the Th1 response by releasing proinflammatory cytokines and cause further tissue damage through the release of nitric oxide. Myeloid cells in the early Th1 response stimulate the proliferative phase of myogenesis through mechanisms mediated by TNF-␣ and IL-6; experimental prolongation of their presence is associated with delayed transition to the early differentiation stage of myogenesis. Subsequent invasion by CD163ϩ /CD206 ϩ M2 macrophages attenuates M1 populations through the release of anti-inflammatory cytokines, including IL-10. M2 macrophages play a major role in promoting growth and regeneration; their absence greatly slows muscle growth following injury or modified use and inhibits muscle differentiation and regeneration. Chronic muscle injury leads to profiles of macrophage invasion and function that differ from acute injuries. For example, mdx muscular dystrophy yields invasion of muscle by M1 macrophages, but their early invasion is accompanied by a subpopulation of M2a macrophages. M2a macrophages are IL-4 receptor ϩ /CD206 ϩ cells that reduce cytotoxicity of M1 macrophages. Subsequent invasion of dystrophic muscle by M2c macrophages is associated with progression of the regenerative phase in pathophysiology. Together, these findings show that transitions in macrophage phenotype are an essential component of muscle regeneration in vivo following acute or chronic muscle damage. skeletal muscle; macrophage; neutrophil; muscular dystrophy; chemokines SKELETAL MUSCLE HAS A REMARKABLE capacity for repair, even following severe damage. Experimental findings show that crushing muscle, killing muscle by the injection of toxins, mechanical destruction caused by large, lengthening stretches, or killing muscle fibers by freezing can be followed by the successful regeneration of muscle that leads to recovery of normal structure and function. The regenerative capacity of skeletal muscle relies largely on the presence of a population of mononucleated, myogenic cells, called satellite cells, that retain their ability to proliferate and then differentiate to either fuse with existing fibers or with other myogenic cells to generate new fibers. Thus, perturbations to the processes that normally regulate the activation, proliferat...

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Section: Do Neutrophil-derived or M1 Macrophage-derived Molecules Modmentioning

confidence: 77%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

907

987

View full text Add to dashboard Cite

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“…1). It is important to note that although this in vivo model measures isometric torque produced by the left anterior crural muscles, the TA comprises 82 % of the muscle group mass and contributes 89 % of the peak torque produced by the muscle group making it a valid assessment of TA muscle function (Lowe et al 1995;Warren et al 2002).…”

Section: Experimental Designmentioning

confidence: 99%

Utility of 17-(allylamino)-17-demethoxygeldanamycin treatment for skeletal muscle injury

Baumann

Rogers

Otis

2016

Cell Stress and Chaperones

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Repeated eccentric contractions can injure skeletal muscle and result in functional deficits that take several weeks to fully recover. The 70-kDa heat shock protein (Hsp70) is a stress-inducible molecular chaperone that maintains protein quality and plays an integral role in the muscle's repair processes following injury. Here, we attempted to hasten this recovery by pharmacologically inducing Hsp70 expression in mouse skeletal muscle with 17-(allylamino)-17-demethoxygeldanamycin (17-AAG) (40 mg/kg) both prior to and throughout the first 7 days after an injurious bout of 150 maximal eccentric contractions. Hsp70 content in the injured skeletal muscle was strongly induced following the eccentric contractions and remained elevated over the next 7 days as the muscle underwent repair. Treatment with 17-AAG increased Hsp70 content ∼five-fold; however, this was significantly less than that induced by the injury. Moreover, 17-AAG treatment did not recover the decrements to in vivo isometric torque production following the bout of eccentric contractions.Together, these findings demonstrate that although Hsp70 content was induced in the uninjured skeletal muscle, treatment of 17-AAG (40 mg/kg) was not a preventive measure to either reduce the severity of skeletal muscle damage or enhance functional recovery following a bout of maximal eccentric contractions.

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“…Two days or more after injury, the levels had normalized. Similarly, Warren et al 8. reported that traumatic skeletal muscle injury is accompanied by an early increase in TNF‐α expression characterized by a single peak that is maximal at 24 hours after injury, as seen using real‐time polymerase chain reaction.…”

Section: Discussionmentioning

confidence: 87%

“…The invasive freeze‐induced model8 and contraction‐induced model of muscle injury9 are well known. However, these models do not closely match clinical observations.…”

mentioning

confidence: 99%

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Muscle injury in rats induces upregulation of inflammatory cytokines in injured muscle and calcitonin gene–related peptide in dorsal root ganglia innervating the injured muscle

et al. 2016

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Introduction: In this study we evaluated the relationships among the behavioral changes after muscle injury, histological changes, changes in inflammatory cytokines in the injured muscle, and changes in the sensory nervous system innervating the muscle in rats. Methods: We established a model of muscle injury in rats using a dropped weight. Behavior was assessed using the CatWalk system. Subsequently, bilateral gastrocnemius muscles and dorsal root ganglia (DRGs) were resected. Muscles were stained with hematoxylin and eosin, and inflammatory cytokines in injured muscles were assayed. DRGs were immunostained for calcitonin gene–related peptide (CGRP). Results: Changes of behavior and upregulation of inflammatory cytokines in injured muscles subsided within 2 days of injury. Repaired tissue was observed 3 weeks after injury. However, upregulation of CGRP in DRG neurons continued for 2 weeks after injury. Conclusion: These findings may explain in part the pathological mechanism of persistent muscle pain. Muscle Nerve 54: 776–782, 2016

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Physiological role of tumor necrosis factor α in traumatic muscle injury

Cited by 226 publications

References 39 publications

Regulatory interactions between muscle and the immune system during muscle regeneration

Regulatory interactions between muscle and the immune system during muscle regeneration

Utility of 17-(allylamino)-17-demethoxygeldanamycin treatment for skeletal muscle injury

Muscle injury in rats induces upregulation of inflammatory cytokines in injured muscle and calcitonin gene–related peptide in dorsal root ganglia innervating the injured muscle

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