TRAF6 regulates satellite stem cell self-renewal and function during regenerative myogenesis

Hindi, Sajedah M.; Kumar, Ashok

doi:10.1172/jci81655

Cited by 66 publications

(105 citation statements)

References 63 publications

(107 reference statements)

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“…By ubiquitinating Pax7, Nedd4-1 shifts the balance in favor of MyoD and promotes myogenesis. Interestingly, the TRAF6 ubiquitin ligase activates ERK1/2 and JNK1/2 in satellite cells, leading to activation of Jun and induction of Pax7, and the knockout of TRAF6 leads to increased Pax7 levels and impaired muscle regeneration (36). This mechanism, along with the observation that TRAF6 is involved in the p38/mitogen-activated protein kinases (MAPK) and Akt pathways, can provide a mechanistic explanation for the impaired myogenesis seen in mice with silenced TRAF6 (120).…”

Section: The Ups Regulates Myogenesismentioning

confidence: 99%

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

Bilodeau

Coyne

Wing

2016

American Journal of Physiology-Cell Physiology

126

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Bilodeau PA, Coyne ES, Wing SS. The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation. Am J Physiol Cell Physiol 311: C392-C403, 2016. First published August 10, 2016; doi:10.1152/ajpcell.00125.2016.-Muscle atrophy complicates many diseases as well as aging, and its presence predicts both decreased quality of life and survival. Much work has been conducted to define the molecular mechanisms involved in maintaining protein homeostasis in muscle. To date, the ubiquitin proteasome system (UPS) has been shown to play an important role in mediating muscle wasting. In this review, we have collated the enzymes in the UPS whose roles in muscle wasting have been confirmed through loss-of-function studies. We have integrated information on their mechanisms of action to create a model of how they work together to produce muscle atrophy. These enzymes are involved in promoting myofibrillar disassembly and degradation, activation of autophagy, inhibition of myogenesis as well as in modulating the signaling pathways that control these processes. Many anabolic and catabolic signaling pathways are involved in regulating these UPS genes, but none appear to coordinately regulate a large number of these genes. A number of catabolic signaling pathways appear to instead function by inhibition of the insulin/IGF-I/protein kinase B anabolic pathway. This pathway is a critical determinant of muscle mass, since it can suppress key ubiquitin ligases and autophagy, activate protein synthesis, and promote myogenesis through its downstream mediators such as forkhead box O, mammalian target of rapamycin, and GSK3␤, respectively. Although much progress has been made, a more complete inventory of the UPS genes involved in mediating muscle atrophy, their mechanisms of action, and their regulation will be useful for identifying novel therapeutic approaches to this important clinical problem.hormones; muscle atrophy SKELETAL MUSCLE SERVES TWO essential functions, a contractile function for locomotion/maintenance of posture and a metabolic function as the protein reservoir of the body. The myofibers that make up the muscle consist primarily of myofibrillar proteins. The ability of the body to maintain posture or to move arises from the precise organization of myofibrillar proteins into a contractile unit called the sarcomere. The sarcomere consists of thick filaments containing primarily myosin that can slide over thin filaments containing primarily actin. Both types of filaments contain additional regulatory proteins and are linked to the ␣-actinin-containing Z disk, the thin filaments directly so and the thick filaments via titin. Vimentin and desmin are intermediate filaments that serve to anchor sarcomeres properly at the Z disks. These myofibrillar proteins, as well as the sarcoplasmic proteins, also serve as the protein reservoir of the body. Upon fasting, once hepatic glycogen stores are depleted, muscle protein degradation must be activated to provide amino acids to the liver for gluconeogenesis. These amino a...

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Section: The Ups Regulates Myogenesismentioning

confidence: 99%

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

Bilodeau

Coyne

Wing

2016

American Journal of Physiology-Cell Physiology

126

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“…In an elegant study, Chen et al have demonstrated that miR-1 and miR-206 target Pax7 mRNA to facilitate satellite cell differentiation [23]. We have recently demonstrated that tumor necrosis factor (TNF) receptor associated factor 6 (TRAF6), an adaptor protein which also functions as an E3 ubiquitin ligase, is an important regulator of satellite cell homeostasis in adult skeletal muscle [34]. TRAF6-mediated signaling is required for the activation of the c-JUN/activator protein 1 transcription factor, which increases the expression of Pax7 in satellite cells [34].…”

Section: Noncoding Rnas In Myogenesismentioning

confidence: 99%

“…We have recently demonstrated that tumor necrosis factor (TNF) receptor associated factor 6 (TRAF6), an adaptor protein which also functions as an E3 ubiquitin ligase, is an important regulator of satellite cell homeostasis in adult skeletal muscle [34]. TRAF6-mediated signaling is required for the activation of the c-JUN/activator protein 1 transcription factor, which increases the expression of Pax7 in satellite cells [34]. Interestingly, lack of TRAF6 dramatically increases the levels of miR-1, miR-133, and miR-206 in cultured myogenic cells and in injured myofibers of satellite-cell specific TRAF6-knockout mice, leading to precocious differentiation of satellite cells.…”

Section: Noncoding Rnas In Myogenesismentioning

confidence: 99%

Noncoding RNAs in the regulation of skeletal muscle biology in health and disease

Simionescu-Bankston

Kumar

2016

J Mol Med

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Skeletal muscle is composed of multinucleated myofibers that arise from the fusion of myoblasts during development. Skeletal muscle is essential for various body functions such as maintaining posture, locomotion, breathing, and metabolism. Skeletal muscle undergoes remarkable adaptations in response to environmental stimuli leading to atrophy or hypertrophy. Moreover, degeneration of skeletal muscle is a common feature in a number of muscular disorders including muscular dystrophy. Emerging evidence suggests that noncoding RNAs, such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are critical for skeletal muscle physiology. Several miRNAs and lncRNAs have now been found to control skeletal muscle development and regeneration. Noncoding RNAs also play an important role in the regulation of skeletal muscle mass in adults. Furthermore, aberrant expression of miRNAs and lncRNAs has been observed in several muscular disorders. In this article, we discuss the mechanisms of action of miRNAs and lncRNAs in skeletal muscle formation, growth, regeneration, and disease. We further highlight potential therapeutic strategies for utilizing noncoding RNAs to improve skeletal muscle function.

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“…Thus, intensive research into tongue development may offer useful clues for the development of novel tongue regeneration strategies based on tissue engineering and stem cell therapy. Previous studies have indicated that muscle regeneration after injury exhibits similarities to muscle development, and that quiescent myogenic cells, also called satellite cells, which are situated beneath the basal lamina that surrounds each myofiber, were activated to proliferate, differentiate and fuse to form multinucleated myofibers (10)(11)(12). Other types of non-muscle stem cells may also participate in this process.…”

Section: Discussionmentioning

confidence: 99%

Histological study of postnatal development of mouse tongues

Jiang¹,

Chen

2017

Exp Ther Med

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Abstract. Numerous factors, including trauma, tumors and myophagism, may lead to tongue defects, which are mostly repaired via muscular flaps. However, these methods cannot restore the muscular function and gustation function of the tongue. Intensive research on tongue development may offer useful clues for tongue regeneration based on tissue engineering or stem cell therapy. In the present study, staining results revealed that tongue muscle fibers became larger, mature and stronger, and the foliate and fungiform papillae also became mature from newborn to adult C57BL/6J genetic background mice. Immunofluorescence staining and polymerase chain reaction results revealed that C-kit was dynamically expressed in muscle cells, as well as in foliate and fungiform papilla cells from newborn to adult stages. The expression level decreased from P1 to P15 and increased at P90. The immunofluorescence staining results revealed that Ki-67 was expressed in muscle cells and papilla cells from newborn to adult stages, and high expression was observed at P6 and P15. In addition, the immunofluorescence staining results also demonstrated that msh homeobox 2 (Msx2) was dynamically expressed in postnatal tongue muscle cells; however, almost no expression was detected in papilla cells. There was relative high expression level of Msx2 at P1 and P6 stages, but this gradually decreased from P15, and it was expressed primarily in the muscle cells located in the marginal zone of the tongue at P90. These findings suggest that the amount of c-kit-expressing precursor cells in tongue muscle and papilla cells increases to promote tongue development at the early postnatal stage and to maintain homeostasis and functional adaptation of the tongue in the adult stage. Furthermore, Msx2 may serve an important role in postnatal tongue muscle development. The present study also suggests that C-kit and Msx2 may be used as cell markers for postnatal tongue regeneration and self-repair, and may provide an approach for developing treatment methods for tongue diseases with a postnatal onset. IntroductionNormal tongue development has a crucial role in craniofacial development, particularly for jaw and palate development (1). Tongue primordium is comprised of mesenchyme cells derived from cranial neural crest cells (CNCCs), ectoderm-derived lingual epithelium in the distal portion and the endoderm-derived proximal portion (2). The myoblasts migrated from the occipital somites surround the CNCCs during the process of tongue development (2). Core myogenic regulators, such as MyoD, myogenic factor (Myf)5 and Myf6 (also known as MRF4) have important roles in tongue muscle development (3). However, the tongue muscle also exhibits unique characteristics that are distinct from those of other skeletal muscles, and different regulatory mechanisms may be in place. Previous studies demonstrated that transforming growth factor β1, Smad4 and fibroblast growth factor 6 signaling pathways regulate myogenic differentiation and myoblast fusion during tongue development (2,3...

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TRAF6 regulates satellite stem cell self-renewal and function during regenerative myogenesis

Cited by 66 publications

References 63 publications

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

Noncoding RNAs in the regulation of skeletal muscle biology in health and disease

Histological study of postnatal development of mouse tongues

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