Urocortins Improve Dystrophic Skeletal Muscle Structure and Function through Both PKA- and Epac-Dependent Pathways

Reutenauer-Patte, Julie; Boittin, François-Xavier; Patthey-Vuadens, O.; Rüegg, Urs T.; Dorchies, O.M.

doi:10.1016/j.ajpath.2011.10.038

Cited by 38 publications

(55 citation statements)

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“…Interestingly, elevated PDE activity is observed in skeletal muscle of dystrophic mice (20,21,143). Although these findings do not imply that reduced cAMP abundance in dystrophic muscle causes the dystrophic phenotype, it would be interesting to test whether chronic PDE inhibition can improve muscle regeneration or function in dystrophic muscle in a manner analogous to ␤ 2 -AR and CRFR2 agonists (90,103,185,254,256). Studies with prolonged PDE inhibitor treatment should be evaluated with caution, as mice lacking Pde4d display exercise intolerance and evidence of myofiber damage after downhill running (17).…”

Section: (See Hypertrophy and Injury And Regeneration)mentioning

confidence: 99%

“…␤ 2 -AR agonists have also been shown to reduce muscle atrophy in animals with cancer cachexia (31,33,46). In addition, agonists for ␤ 2 -AR or CRF receptors improve muscle function in dystrophin-deficient mdx (86,90,103,185,192,254,256) and laminin-deficient dy/dy (94) mice. However, efficacy of ␤ 2 -AR agonists on muscle size and force generation vary with the type and dose of agonist, as well as the muscle studied.…”

Section: Camp In Functional Adaptation Of Skeletal Musclementioning

confidence: 99%

“…Several proteins involved in cAMP signaling, including receptors, G proteins, and cAMP-activated transcription factors, have been found to promote muscle regeneration (80,163,216) and functional recovery after injury (15,196). Ligands for these GPCRs also improve muscle function and slow disease progression in dystrophic mdx mice (86,90,103,185,192,254,256). In conjunction with the anti-atrophy effects described in the preceding section (see Hypertrophy), GPCR signaling in muscle precursor cells is a potential area for development of novel therapeutic agents that could promote regeneration and limit atrophy in patients with muscular dystrophy, denervation atrophy, age-related sarcopenia, or muscle wasting due to cancer.…”

Section: Camp In Muscle Development and Regenerationmentioning

confidence: 99%

“…The prohypertrophic actions of ␤-adrenergic receptor (␤-AR) agonists and corticotropin-releasing factor receptor 2 (CRFR2) agonists have recently been harnessed to improve muscle function and ameliorate atrophy in several rodent models, including disuse (99, 101, 245), denervation (98, 100 -102, 127, 154, 253), aging (195, 254), and muscular dystrophy (90,103,185,254,256). ␤-AR agonists have also shown some promise in promoting muscle function in patients with muscular dystrophy (64,125,126,211, 235).…”

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cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

Berdeaux

Stewart

2012

American Journal of Physiology-Endocrinology and Metabolism

153

115

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Berdeaux R, Stewart R. cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration. Am J Physiol Endocrinol Metab 303: E1-E17, 2012. First published February 21, 2012 doi:10.1152/ajpendo.00555.2011.-Among organ systems, skeletal muscle is perhaps the most structurally specialized. The remarkable subcellular architecture of this tissue allows it to empower movement with instructions from motor neurons. Despite this high degree of specialization, skeletal muscle also has intrinsic signaling mechanisms that allow adaptation to long-term changes in demand and regeneration after acute damage. The second messenger adenosine 3=,5=-monophosphate (cAMP) not only elicits acute changes within myofibers during exercise but also contributes to myofiber size and metabolic phenotype in the long term. Strikingly, sustained activation of cAMP signaling leads to pronounced hypertrophic responses in skeletal myofibers through largely elusive molecular mechanisms. These pathways can promote hypertrophy and combat atrophy in animal models of disorders including muscular dystrophy, agerelated atrophy, denervation injury, disuse atrophy, cancer cachexia, and sepsis. cAMP also participates in muscle development and regeneration mediated by muscle precursor cells; thus, downstream signaling pathways may potentially be harnessed to promote muscle regeneration in patients with acute damage or muscular dystrophy. In this review, we summarize studies implicating cAMP signaling in skeletal muscle adaptation. We also highlight ligands that induce cAMP signaling and downstream effectors that are promising pharmacological targets. cyclic AMP; skeletal muscle; cell signaling; muscle regeneration; atrophy; protein kinase A ORIGINALLY DISCOVERED by Sutherland and Rall in liver homogenates in 1958 (218), adenosine 3=,5=-monophosphate (cyclic AMP, or cAMP) has since been intensively studied and is one of the best-characterized signaling molecules. In skeletal muscle, acute cAMP signaling has been implicated in regulation of glycogenolysis (213), contractility (32,83,84,88,138,234), sarcoplasmic calcium dynamics (58,147,184,204), and recovery from sustained contractile activity (44, 162). The net result of acute cAMP action on the order of minutes in skeletal muscle can generally be described as increased contractile force and rapid recovery of ion balance, especially during prolonged contractions. These acute changes are most pertinent to muscle contraction and energy utilization during exercise, when epinephrine is rapidly released into the circulation (92) and cAMP accumulates in muscle (72).Many studies have shown, however, that cAMP-inducing agents or genetic modification of proteins involved in cAMP signaling can also have adaptive effects on skeletal muscle by increasing myofiber size and promoting fiber-type transitions to glycolytic fibers (9,18,42,43,57,63,86,91,101,121,128,154,155,163,190,193,194,215). The prohypertrophic actions of ␤-adrenergic receptor (␤-AR) agonists and corticotropin-releasing factor recept...

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Section: (See Hypertrophy and Injury And Regeneration)mentioning

confidence: 99%

Section: Camp In Functional Adaptation Of Skeletal Musclementioning

confidence: 99%

Section: Camp In Muscle Development and Regenerationmentioning

confidence: 99%

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confidence: 99%

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cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

Berdeaux

Stewart

2012

American Journal of Physiology-Endocrinology and Metabolism

153

115

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“…Notably, in dystrophic mdx mice treatment with urocortins significantly ameliorated a set of symptoms, ranging from fiber necrosis to muscle function. Possible mechanisms of action might include cAMPinduced activation of PKA and Epac, which in turn may address altered Ca 2+ handling in skeletal muscle fibers (Reutenauer-Patte et al, 2012).…”

Section: Pka Microdomains At the Sarcomeric Regionmentioning

confidence: 99%

Interação funcional entre o sistema colinérgico e adrenérgico na manutenção da massa muscular e da placa motora

Borges¹

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Combined XIL‐6R and urocortin‐2 treatment restores MDX diaphragm muscle force

et al. 2017

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Urocortins Improve Dystrophic Skeletal Muscle Structure and Function through Both PKA- and Epac-Dependent Pathways

Cited by 38 publications

References 54 publications

cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

Interação funcional entre o sistema colinérgico e adrenérgico na manutenção da massa muscular e da placa motora

Combined XIL‐6R and urocortin‐2 treatment restores MDX diaphragm muscle force

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