Factors involved in strain-induced injury in skeletal muscles and outcomes of prolonged exposures

Stauber, William T.

doi:10.1016/j.jelekin.2003.09.010

Cited by 59 publications

(35 citation statements)

References 115 publications

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“…Repetitive strain or trauma produces muscle inflammation that may lead to pain (Yassi, 1997, Melhorn, 1998, Latko et al, 1999, Stauber, 2004, which may re-emerge months or even years after the initial injury (Tjepkema, 2003). We have previously shown that intradermal administration of carrageenan produces cutaneous hyperalgesia, and following complete recovery of nociceptive threshold, hyperalgesia produced by subsequent administration of inflammatory mediators is significantly longer than that produced in naïve controls (Aley et al, 2000, Dina et al, 2003, Parada et al, 2003b.…”

Section: Introductionmentioning

confidence: 99%

“…While we have shown that chronic latent hyperalgesia can be induced in the skin, chronic pain in muscle and other deep somatic tissue is clinically more common and refractory to existing therapies (Mense, 2003). Since chronic muscle pain is believed to be dependent, at least in part, on muscle inflammation (Barr and Barbe, 2002, Stauber, 2004, Sluka et al, 2007, we have recently developed a model of chronic latent muscle hyperalgesia wherein intramuscular administration of carrageenan produces hyperalgesia (lasting ~3 days), and following complete recovery of nociceptive threshold hyperalgesia produced by intramuscular injections of the inflammatory mediator prostaglandin E 2 (PGE 2 ) induced mechanical hyperalgesia that was markedly prolonged compared to control animals (Dina, O. et al, submitted). Since the pronociceptive cytokine interleukin (IL) 6 is produced in muscle exposed to carrageenan (Loram et al, 2007), we investigated whether chronic latent muscle hyperalgesia develops following transient inflammation induced by IL-6.…”

Section: Introductionmentioning

confidence: 99%

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Role of interleukin-6 in chronic muscle hyperalgesic priming

2008

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After recovery from acute muscle pain even minor subsequent muscle use can initiate recurrence of the same mechanical hyperalgesia months or years after the initial injury. We have recently developed a model of this chronic latent hyperalgesia in the rat. In this study, we have examined the possibility that IL-6, an inflammatory mediator produced during acute muscle inflammation, can mediate the production of this chronic latent hyperalgesic state in which subsequent exposure to inflammatory mediators produce a markedly prolonged mechanical hyperalgesia. We now report that intramuscular injection of IL-6 produced mechanical hyperalgesia, lasting several hours, that was prevented by intrathecal injection of antisense to gp130, an IL-6 receptor subunit. Furthermore, following complete recovery from intramuscular IL-6-induced hyperalgesia, intramuscular PGE 2 produced a mechanical hyperalgesia that was remarkably prolonged compared to naïve controls, indicating the presence of chronic latent hyperalgesia. This ability of IL-6 to produce chronic latent hyperalgesia was prevented by intrathecal admininstration of antisense for gp130. Furthermore, gp130 antisense also prevented chronic latent hyperalgesia produced by intramuscular injection of the inflammogen, carrageenan. These results identify a role for IL-6 in acute inflammatory muscle pain and as a potential target against which therapies might be directed to treat chronic muscle pain.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of interleukin-6 in chronic muscle hyperalgesic priming

2008

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“…Chronic musculoskeletal pain conditions such as repetitive strain injury and tendonitis are clearly associated with peripheral tissue damage that includes inflammation of the muscle (Barr and Barbe, 2002;Barr et al, 2004;Stauber, 2004). Data from the Bureau of Labor and Statistics states that 53% of the private workforce had musculoskeletal pain over the last 2 weeks, and 13% of these lost productive work time with losses estimated at $61 billion per year.…”

Section: Introductionmentioning

confidence: 99%

ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation

Sluka

Radhakrishnan

Benson

et al. 2007

Pain

166

160

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Peripheral initiators of muscle pain are virtually unknown, but likely key to development of chronic pain after muscle insult. The current study tested the hypothesis that ASIC3 in muscle is necessary for development of cutaneous mechanical, but not heat hyperalgesia induced by muscle inflammation. Using mechanical and heat stimuli, we assessed behavioral responses in ASIC3−/− and ASIC3+/+ mice after induction of carrageenan muscle inflammation. ASIC3−/−mice did not develop cutaneous mechanical hyperalgesia after muscle inflammation when compared to ASIC3+/ + mice; heat hyperalgesia developed similarly between groups. We then tested if the phenotype could be rescued in ASIC3−/− mice by using a recombinant herpes virus vector to express ASIC3 in skin (where testing occurred) or muscle (where inflammation occurred). Infection of mouse DRG neurons with ASIC3-encoding virus resulted in functional expression of ASICs. Injection of ASIC3-encoding virus into muscle or skin of ASIC3−/− mice resulted in ASIC3 mRNA in DRG and protein expression in DRG and the peripheral injection site. Injection of ASIC3-encoding virus into muscle, but not skin, resulted in development of mechanical hyperalgesia similar to that observed in ASIC3+/+ mice. Thus, ASIC3 in primary afferent fibers innervating muscle is critical to development of hyperalgesia that results from muscle insult.

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“…2,6,24 However, muscle healing is impeded with fibrosis formation and chronic pain if the inflammatory reaction is extended (chronic inflammation), which often occurs during the healing of aged muscle or severely injured muscle. 2,6,[25][26] Therefore, inflammatory reaction and fibrotic scar formation are required to be balanced or controlled for muscle healing.…”

mentioning

confidence: 99%

Relaxin Regulates MMP Expression and Promotes Satellite Cell Mobilization During Muscle Healing in Both Young and Aged Mice

Urso

Murray

et al. 2010

The American Journal of Pathology

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The polypeptide hormone relaxin has been proven to be effective in promoting both the remodeling and regeneration of various tissues, including cardiac muscle. In addition, our previous study demonstrated that relaxin is beneficial to skeletal muscle healing by both promoting muscle regeneration and preventing fibrosis formation. However, the molecular and cellular mechanisms of relaxin in regulating both myogenic cell differentiation and muscle healing process are still unclear. In this study, C2C12 mouse myoblasts and primary human myoblasts were treated with relaxin to investigate its potential effect in vitro; relaxin was also injected intramuscularly into the injured site of the mouse on the second day after injury to observe its function in vivo, especially in the aged muscle. Results showed that relaxin promoted myogenic differentiation, migration, and activation of matrix metalloproteinases (MMPs) of cultured myoblasts in vitro. In the injured muscle, relaxin administration promoted the activation of Pax7-positive skeletal muscle satellite cells and increased its local population compared with nontreated control muscles. Meanwhile, both angiogenesis and revascularization were increased, while the extended inflammatory reaction was repressed in the relaxin-treated injured muscle. Moreover, relaxin similarly promoted muscle healing in mice with aged muscle. These results revealed the multiple effects of relaxin in systematically improving muscle healing as well as its potential for clinical applications in patients with skeletal muscle injuries and diseases. (Am J Pathol

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Factors involved in strain-induced injury in skeletal muscles and outcomes of prolonged exposures

Cited by 59 publications

References 115 publications

Role of interleukin-6 in chronic muscle hyperalgesic priming

Role of interleukin-6 in chronic muscle hyperalgesic priming

ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation

Relaxin Regulates MMP Expression and Promotes Satellite Cell Mobilization During Muscle Healing in Both Young and Aged Mice

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