Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy

Jackson, Janna R.; Mula, Jyothi; Kirby, Tyler J.; Fry, Christopher S.; Lee, Jonah D.; Ubele, Margo F.; Campbell, Kenneth S.; McCarthy, John J.; Peterson, Charlotte A.; Dupont‐Versteegden, Esther E.

doi:10.1152/ajpcell.00207.2012

Cited by 130 publications

(130 citation statements)

References 31 publications

(48 reference statements)

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“…These findings raise the question of whether satellite cells are necessary for muscle hypertrophy, at least the amount that is generally elicited with exercise-training paradigms used for health and wellness of older individuals and the treatment of sarcopenia. This general question has been debated recently (63,76), and the answer is apparently not yet at hand (46,60,83).…”

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confidence: 99%

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Trappe

Liu

2013

Journal of Applied Physiology

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Trappe TA, Liu SZ. Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise. J Appl Physiol 115: 909 -919, 2013. First published March 28, 2013 doi:10.1152/japplphysiol.00061.2013.-It has been ϳ40 yr since the discovery that PGs are produced by exercising skeletal muscle and since the discovery that inhibition of PG synthesis is the mechanism of action of what are now known as cyclooxygenase (COX)-inhibiting drugs. Since that time, it has been established that PGs are made during and after aerobic and resistance exercise and have a potent paracrine and autocrine effect on muscle metabolism. Consequently, it has also been determined that orally consumed doses of COX inhibitors can profoundly influence muscle PG synthesis, muscle protein metabolism, and numerous other cellular processes that regulate muscle adaptations to exercise loading. Although data from acute human exercise studies, as well as animal and cell-culture data, would predict that regular consumption of a COX inhibitor during exercise training would dampen the typical muscle adaptations, the chronic data do not support this conjecture. From the studies in young and older individuals, lasting from 1.5 to 4 mo, no interfering effects of COX inhibitors on muscle adaptations to resistance-exercise training have been noted. In fact, in older individuals, a substantial enhancement of muscle mass and strength has been observed. The collective findings of the PG/COX-pathway regulation of skeletal muscle responses and adaptations to exercise are compelling. Considering the discoveries in other areas of COX regulation of health and disease, there is certainly an interesting future of investigation in this re-emerging area, especially as it pertains to older individuals and the condition of sarcopenia, as well as exercise training and performance of individuals of all ages. PGE 2; PGF2␣; acetaminophen; ibuprofen; sarcopenia PGS PRODUCED BY the cyclooxygenase (COX) enzyme are ubiquitous in human physiology and regulate numerous processes (105, 108), including muscle protein metabolism (78,93,106,126,128). As a result, PGs regulate adaptations to muscular exercise, and COX-inhibiting drugs can alter the acute and chronic responses to exercise. Because of the continuum of acute responses and chronic adaptations that exists from lowerintensity, longer-duration exercise to higher-intensity, shorterduration exercise, it is difficult to adopt a "one-mechanismfits-all" approach to PG and COX involvement in skeletal muscle exercise adaptations. This is also true when distinguishing between muscle injury and muscular exercise for health and performance.COX-inhibiting drugs are one of the most commonly consumed classes of drugs in the world. In the United States, the COX inhibitors, acetaminophen, ibuprofen, and aspirin, are the top three consumed drugs of young, middle-aged, and older individuals, with ϳ50 million individuals using each of these drugs during any given week (52, 129). Interestingly, two of these drugs (acetaminophen...

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confidence: 99%

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Trappe

Liu

2013

Journal of Applied Physiology

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“…The effect of satellite cell ablation on skeletal muscle regrowth following atrophy was also reported 15) . Adult tamoxifen-inducible Pax7-DTA mice were subjected to either 2 weeks of hindlimb suspension to induce muscular atrophy or 2 weeks of hindlimb suspension followed by 2 weeks of reloading to allow regrowth.…”

Section: Role Of Satellite Cells In Muscular Hypertrophy and Regrowthmentioning

confidence: 95%

Role of satellite cells in skeletal muscle plasticity: Beyond muscle regeneration

Tamura

Furuichi

Manabe

et al. 2017

JPFSM

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Satellite cells are resident muscle stem cells located between the basal lamina and the plasma membrane of myofibers. They play crucial roles in muscle growth during the postnatal stage and muscle regeneration following postnatal development. However, the roles of satellite cells in adult muscles -in muscle growth, function, and adaptation -are poorly understood. Recently, by studying genetically engineered mice with conditionally ablated satellite cells, it has been reported that satellite cells play important roles in muscle growth and maintenance of muscle spindles or neuromuscular junctions, and produce growth factors that affect other organs. Here, we review the recent studies using tamoxifen-inducible Pax7-DTA mice and describe the novel roles of satellite cells in the maintenance of skeletal muscle plasticity.

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“…However, Jackson et al (18) reported that myonuclear number in transgenic Pax7-DTA mice with depletion of satellite cells (Ͼ90%) following administration of tamoxifen did not change in response to hind limb unloading and reloading, but atrophy and regrowth of soleus were induced following 14 days of unloading and reloading. Therefore, muscle atrophy caused by hind limb unloading may be recovered because the basal myonuclear number was maintained.…”

Section: Responses To Reloadingmentioning

confidence: 99%

“…The same group as Jackson et al (18) studied the responses of muscle fiber size to functional overloading in transgenic Pax7-DTA mice with depletion of satellite cells following administration of tamoxifen (15,29). In response to 2-wk overloading, hypertrophy was induced in plantaris, although myonuclear number did not change (29).…”

Section: Responses To Reloadingmentioning

confidence: 99%

“…Satellite cells have been shown to serve as a source of new myonuclei during regeneration after a muscle injury (31,50,52) and during functional overload (10,15,30,53), although it was also reported that overload-related hypertrophy and/or regrowth of atrophied muscle were not inhibited by depletion of satellite cells following administration of tamoxifen (18,29).…”

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Macrophage deficiency in osteopetrotic (op/op) mice inhibits activation of satellite cells and prevents hypertrophy in single soleus fibers

Ohira

Wang

Ito

et al. 2015

American Journal of Physiology-Cell Physiology

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Effects of macrophage on the responses of soleus fiber size to hind limb unloading and reloading were studied in osteopetrotic homozygous (op/op) mice with inactivated mutation of macrophage colony-stimulating factor (M-CSF) gene and in wild-type (ϩ/ϩ) and heterozygous (ϩ/op) mice. The basal levels of mitotically active and quiescent satellite cell (Ϫ46 and Ϫ39% vs. ϩ/ϩ, and Ϫ40 and Ϫ30% vs. ϩ/op) and myonuclear number (Ϫ29% vs. ϩ/ϩ and Ϫ28% vs. ϩ/op) in fibers of op/op mice were significantly less than controls. Fiber length and sarcomere number in op/op were also less than ϩ/ϩ (Ϫ22%) and ϩ/op (Ϫ21%) mice. Similar trend was noted in fiber cross-sectional area (CSA, Ϫ15% vs. ϩ/ϩ, P ϭ 0.06, and Ϫ14% vs. ϩ/op, P ϭ 0.07). The sizes of myonuclear domain, cytoplasmic volume per myonucleus, were identical in all types of mice. The CSA, length, and the whole number of sarcomeres, myonuclei, and mitotically active and quiescent satellite cells, as well as myonuclear domain, in single muscle fibers were decreased after 10 days of unloading in all types of mice, although all of these parameters in ϩ/ϩ and ϩ/op mice were increased toward the control values after 10 days of reloading. However, none of these levels in op/op mice were recovered. Data suggest that M-CSF and/or macrophages are important to activate satellite cells, which cause increase of myonuclear number during fiber hypertrophy. However, it is unclear why their responses to general growth and reloading after unloading are different. myonuclei; muscle fiber size; osteopetrotic mice; satellite cells; unloading and reloading SKELETAL MUSCLES ARE COMPOSED of multinucleated muscle fibers and have an extensive capacity for morphological and functional adaptation. For example, chronic unloading of muscles by bedrest in humans (45,46,64) and hind limb suspension and actual spaceflight in animals (6, 40 -42, 47, 59) result in muscle fiber atrophy and a shift toward a faster myosin heavy chain profile, particularly in antigravity muscles composed predominantly of slow-twitch fibers, such as the soleus (6,42,(45)(46)(47) and adductor longus (41, 59). Muscle fiber atrophy and the shift toward a faster myosin heavy chain profile are reversed in response to muscle reloading (41,45,46,59). The muscular response to reloading appears to be closely related to intramuscular stimuli that are activated by mechanical loading (20,21,41,47,59) and/or muscle activation with reloading (1,12,20,22,41).Macrophage colony-stimulating factor (M-CSF, CSF-1) is a cytokine that influences hematopoietic stem cells to differentiate into macrophages and other cell types (54). Deficiency of macrophages has been well-reported in osteopetrotic (op/op) mutant mice with inactivating mutation of M-CSF gene, which results in the absence of certain macrophage and in osteopetrosis, following a lack of osteoclasts (60, 63). Tidball and Wehling-Henricks (58) reported important roles of macrophages in the repair of muscle fiber membrane, regeneration, and regrowth after unloading-related atrophy in mouse s...

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Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy

Cited by 130 publications

References 31 publications

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Role of satellite cells in skeletal muscle plasticity: Beyond muscle regeneration

Macrophage deficiency in osteopetrotic (op/op) mice inhibits activation of satellite cells and prevents hypertrophy in single soleus fibers

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