Skeletal muscle response to tenotomy

Jamali, Amir A.; Afshar, Pouya Farokhnezhad; Abrams, Reid A.; Lieber, Richard L.

doi:10.1002/(sici)1097-4598(200006)23:6<851::aid-mus3>3.0.co;2-a

Cited by 92 publications

(75 citation statements)

References 60 publications

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“…The muscle atrophy observed in the Botox mice exceeded that induced by non-surgical models of disuse such as hindlimb suspension [32], but was similar to that observed in more invasive tenotomy and neurectomy models [16,45]. As well, bone loss in the Botox mice was more severe than that observed in C57 mice challenged by hindlimb suspension [18].…”

Section: Discussionmentioning

confidence: 66%

Botox induced muscle paralysis rapidly degrades bone

Warner

Sanford

Becker

et al. 2006

Bone

180

193

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The means by which muscle function modulates bone homeostasis is poorly understood. To begin to address this issue, we have developed a novel murine model of unilateral transient hindlimb muscle paralysis using botulinum toxin A (Botox). Female C57BL/6 mice (16 weeks) received IM injections of either saline or Botox (n = 10 each) in both the quadriceps and calf muscles of the right hindleg. Gait dysfunction was assessed by multi-observer inventory, muscle alterations were determined by wet mass, and bone alterations were assessed by micro-CT imaging at the distal femur, proximal tibia, and tibia mid-diaphysis. Profound degradation of both muscle and bone was observed within 21 days despite significant restoration of weight bearing function by 14 days. The muscle mass of the injected quadriceps and calf muscles was diminished −47.3% and −59.7%, respectively, vs. saline mice (both P < 0.001). The ratio of bone volume to tissue volume (BV/TV) within the distal femoral epiphysis and proximal tibial metaphysis of Botox injected limbs was reduced −43.2% and −54.3%, respectively, while tibia cortical bone volume was reduced −14.6% (all P < 0.001). Comparison of the contralateral non-injected limbs indicated the presence of moderate systemic effects in the model that were most probably associated with diminished activity following muscle paralysis. Taken as a whole, the micro-CT data implied that trabecular and cortical bone loss was primarily achieved by bone resorption. These data confirm the decisive role of neuromuscular function in mediating bone homeostasis and establish a model with unique potential to explore the mechanisms underlying this relation. Given the rapidly expanding use of neuromuscular inhibitors for indications such as pain reduction, these data also raise the critical need to monitor bone loss in these patients.

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Section: Discussionmentioning

confidence: 66%

Botox induced muscle paralysis rapidly degrades bone

Warner

Sanford

Becker

et al. 2006

Bone

180

193

View full text Add to dashboard Cite

show abstract

“…Therefore, the primary goal of this study was to evaluate the effect of 20E on the activation of the UPS in rat skeletal muscle atrophy induced by Achilles tendon transection. The reason behind our selecting this animal model is that this type of atrophy is very commonly encountered by clinicians following orthopedic surgery or degenerative musculoskeletal diseases (18); moreover, tenotomy is reproducible in inducing muscle atrophy. Additionally, there is accumulating evidence that slow-twitch fibers are more sensitive to inactivity or microgravity than fast-twitch fibers (19,20), and 20E enhances muscle hypertrophy of different fiber types in a muscle-specific fashion (15).…”

Section: An Ecdysteroid Hormone Which Controls Molting and Reproductimentioning

confidence: 99%

Effect of 20-Hydroxyecdysone on Proteolytic Regulation in Skeletal Muscle Atrophy

Hirunsai

Yimlamai

Suksamrarn

2016

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Abstract. Skeletal muscle atrophy is a debilitating condition associated with a variety of pathological conditions (e.g. diabetes mellitus, cancer, chronic obstructive pulmonary disease, and chronic heart failure), physiological consequence of aging (sarcopenia), and disuse (e.g. casting-immobilization, microgravity, or tendon injury), subsequently leading to a decrease in mobility and reduced quality of life (1). Muscle atrophy is characterized by a decrease of protein content leading to a reduction in cross-sectional area (CSA) of muscle fibers and impairment of muscle force generation and fatigue resistance (2, 3). Skeletal muscle mass is determined by the balance of protein synthesis and protein breakdown. However, previous compelling evidence has indicated that disuse muscle atrophy is primarily caused by the increase in the rate of protein degradation rather than a decrease in the rate of protein synthesis (4). Although several proteolytic systems are involved in protein turnover in skeletal muscle, recent studies suggested that the ubiquitin-proteasome system (UPS) represents the major intracellular proteolysis machinery responsible for the degradation of major contractile proteins, and contributes significantly to muscle atrophy in both animal and human models (1, 5).To date, in spite of many attempts, there is no single effective method to completely cure muscle atrophy. Although several pharmacological agents such as β2-adrenergic agonist or proteasome inhibitors have been prescribed to combat muscle atrophy (5), these drugs do not come without side-effects. Therefore, a search for a nonpharmacological therapeutic strategy should be considered as an alternative approach to tackle these clinical problems. There is evidence that ecdysteroids, insect hormones, have an anabolic effect on skeletal muscle (6) with no side-effects in mammals, including humans (7).Ecdysteroids act as molting hormones in insects and also play a defensive role against insect herbivory in plants (8).There are a large number of structurally related ecdysteriods in plants (phytoecdysteriods). Of these, 20-hydroxyecdysone (20E) is the most commonly found and extensively studied. This compound is present at high concentration in the bark of blackberry tree (Vitex glabrata). 20E has low toxicity in mammals: the lethal dose 50 (LD 50 ) is 6.4 g/kg in mice for intraperitoneal injection and more than 9 g/kg when given orally (9). The pharmacokinetics of 20E depend on the mode of administration, for example, the half-time of elimination of this substance in lambs when administered via oral, intravenous, and intramuscular routes were 0.2, 0.4, and 2 h, respectively (10). It has been reported that the half-life of

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“…Tendon release induces a broad range of adaptations in the muscle, with reduced muscle length most frequently described 7. Regulation of muscle length occurs by adding (longitudinal hypertrophy) or removing (longitudinal atrophy) contractile material (i.e., sarcomeres) at the ends of myofibrils8 and it has been shown that tendon release leads to a reduced number of sarcomeres in series 9.…”

mentioning

confidence: 99%

Costamere protein expression and tissue composition of rotator cuff muscle after tendon release in sheep

Ruoss

Möhl

Benn

et al. 2017

Journal Orthopaedic Research

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Previous studies suggested that degradation of contractile tissue requires cleavage of the costamere, a structural protein complex that holds sarcomeres in place. This study examined if costamere turnover is affected by a rotator cuff tear in a previously established ovine model. We found the activity of focal adhesion kinase (FAK), a main regulator of costamere turnover, was unchanged at 2 weeks but decreased by 27% 16 weeks after surgical release of the infraspinatus tendon. This was accompanied by cleavage of the costamere protein talin into a 190 kDa fragment while full length talin remained unchanged. At 2 weeks after tendon release, muscle volume decreased by 17 cm3 from an initial 185 cm3, the fatty tissue volume was halved, and the contractile tissue volume remained unchanged. After 16 weeks, the muscle volume decreased by 36 cm3, contractile tissue was quantitatively lost, and the fat content increased by 184%. Nandrolone administration mitigated the loss of contractile tissue by 26% and prevented fat accumulation, alterations in FAK activity, and talin cleavage. Taken together, these findings imply that muscle remodeling after tendon release occurs in two stages. The early decrease of muscle volume is associated with reduction of fat; while, the second stage is characterized by substantial loss of contractile tissue accompanied by massive fat accumulation. Regulation of costamere turnover is associated with the loss of contractile tissue and seems to be impacted by nandrolone treatment. Clinically, the costamere may represent a potential intervention target to mitigate muscle loss after a rotator cuff tear. © 2017 The Authors. Journal of Orthopaedic Research® published by Wiley Periodicals, Inc. on behalf of the Orthopaedic Research Society. J Orthop Res 36:272–281, 2018.

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Skeletal muscle response to tenotomy

Cited by 92 publications

References 60 publications

Botox induced muscle paralysis rapidly degrades bone

Botox induced muscle paralysis rapidly degrades bone

Effect of 20-Hydroxyecdysone on Proteolytic Regulation in Skeletal Muscle Atrophy

Costamere protein expression and tissue composition of rotator cuff muscle after tendon release in sheep

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