Smad4 restricts differentiation to promote expansion of satellite cell derived progenitors during skeletal muscle regeneration

Paris, Nicole D.; Soroka, Andrew; Klose, Alanna; Liu, Wenxuan; Chakkalakal, Joe V.

doi:10.7554/elife.19484

Cited by 33 publications

(51 citation statements)

References 47 publications

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“…IGF-1 affects the balance between protein synthesis and protein degradation thus inducing muscle hypertrophy, whereas TGFβ negatively controls muscle growth (Schiaffino et al, 2013). Interestingly, recent studies demonstrated a new role for the TGFβ/Smad pathway in satellite cell expansion (Paris et al, 2016) and differentiation . During the final steps of muscle remodelling the vasculature and innervation patterns are restored and new MuSCs are set aside.…”

Section: Cellular Regulators Of Muscle Repair and Their Regenerative mentioning

confidence: 99%

Regulation and phylogeny of skeletal muscle regeneration

Baghdadi

Tajbakhsh

2018

Developmental Biology

159

135

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One of the most fascinating questions in regenerative biology is why some animals can regenerate injured structures while others cannot. Skeletal muscle has a remarkable capacity to regenerate even after repeated traumas, yet limited information is available on muscle repair mechanisms and how they have evolved. For decades, the main focus in the study of muscle regeneration was on muscle stem cells, however, their interaction with their progeny and stromal cells is only starting to emerge, and this is crucial for successful repair and reestablishment of homeostasis after injury. In addition, numerous murine injury models are used to investigate the regeneration process, and some can lead to discrepancies in observed phenotypes. This review addresses these issues and provides an overview of the some of the main regulatory cellular and molecular players involved in skeletal muscle repair.Key words: skeletal muscle, regeneration, stem cells, evolution, quiescence, injury IntroductionThe ability to regenerate tissues and structures is a prevalent feature of metazoans although there is significant variability among species ranging from limited regeneration of a tissue (birds and mammals) to regeneration involving the entire organism (cnidarians, planarians, hydra). The intriguing evolutionary loss of regenerative capacity in more complex organisms highlights the importance of identifying the underlying mechanisms responsible for these diverse regenerative strategies. One of the most studied tissues that contributes to new appendage formation is skeletal muscle, thereby making it a major focus of regeneration studies during evolution. The emergence of new lineage-tracing tools in different animal models has permitted the identification of specific progenitor cell populations and their contribution to tissue repair.Skeletal muscles allow voluntary movement and they play a key role in regulating metabolism and homeostasis in the organism. In mice and humans this tissue represents about 30-40% of the total body mass. This tissue provides an excellent tractable model to study regenerative myogenesis and the relative roles of stem and stromal cells following a single, or repeated rounds of injury. Although muscle regeneration relies mainly on its resident muscle stem (satellite) cells (MuSCs) to effect muscle repair, interactions with neighbouring stromal cells, by direct contact or via the release of soluble factors, is essential to restore proper 3 function. Each step of the myogenic process is regulated by specific regulatory factors including extrinsic cues, yet the nature and source of these signals remain unclear. This review will address these issues and discuss the different experimental models used to investigate the regenerative process. Prenatal and postnatal skeletal muscle developmentIn amniotes, skeletal muscles in the limbs and trunk arise from somites through a series of successive waves that include embryonic and foetal phases of myoblast production (Biressi et al., 2007;Comai and Tajbakhsh, 201...

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Section: Cellular Regulators Of Muscle Repair and Their Regenerative mentioning

confidence: 99%

Regulation and phylogeny of skeletal muscle regeneration

Baghdadi

Tajbakhsh

2018

Developmental Biology

159

135

View full text Add to dashboard Cite

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“…To examine growth capacity, FACS‐purified SCs from castrated and sham muscles were plated at low density (30 cells per well) in a clonal growth assay. Cultures of 100 FACS‐purified SCs or less can identify a deficit in the clonal growth capacity of aged SCs [2,6,31]. We found no significant difference in clonal growth between SCs derived from sham or castrated skeletal muscles (Figure 2A, B).…”

Section: Resultsmentioning

confidence: 89%

“…The skin overlaying the tibialis anterior (TA) muscle was then carefully shaved. The TA was directly injected with a 1.2% solution of BaCl 2 in normal saline [2]. At 28 days post-injury, injured and contralateral (uninjured) TAs were collected.…”

Section: Skeletal Muscle Injury and Regenerationmentioning

confidence: 99%

“…Skeletal muscle possesses a remarkable capacity for regeneration, which is mediated by adult resident stem/progenitor cell populations that contribute to repair and maintenance [1–4]. Resident Pax7‐expressing muscle stem cells (satellite cells (SCs)) function as an essential source of myonuclei for the early growth, regeneration and lifelong maintenance of skeletal muscle [2–5]. In adults, most SCs reside in a quiescent state at the interface between the muscle fiber (myofiber) and basal lamina [6,7].…”

Section: Introductionmentioning

confidence: 99%

“…In adults, most SCs reside in a quiescent state at the interface between the muscle fiber (myofiber) and basal lamina [6,7]. In response to a degenerative injury, SCs activate and divide to produce myogenic progenitors for myofiber regeneration [2,8,9]. Effective maintenance and responsiveness of quiescent SCs at homeostasis is required for the preservation of skeletal muscle integrity and regenerative potential [4,10].…”

Section: Introductionmentioning

confidence: 99%

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Castration induces satellite cell activation that contributes to skeletal muscle maintenance

Klose

Liu

Paris

et al. 2018

JCSM Rapid Communications

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Background Sarcopenia, the age-related loss of skeletal muscle, is a side effect of androgen deprivation therapy (ADT) for prostate cancer patients. Resident stem cells of skeletal muscle, satellite cells (SCs), are an essential source of progenitors for the growth and regeneration of skeletal muscle. Decreased androgen signaling and deficits in the number and function of SCs are features of aging. Although androgen signaling is known to regulate skeletal muscle, the cellular basis for ADT-induced exacerbation of sarcopenia is unknown. Furthermore, the consequences of androgen deprivation on SC fate in adult skeletal muscle remain largely unexplored. Methods We examined SC fate in an androgen-deprived environment using immunofluorescence and fluorescence-activated cell sorting (FACS) with SC-specific markers in young castrated mice. To study the effects of androgen deprivation on SC function and skeletal muscle regenerative capacity, young castrated mice were subjected to experimental regenerative paradigms. SC-derived-cell contributions to skeletal muscle maintenance were examined in castrated Pax7CreER/+; ROSA26mTmG/+ mice. SCs were depleted in Pax7CreER/+; ROSA26DTA/+ mice to ascertain the consequences of SC ablation in sham and castrated skeletal muscles. Confocal immunofluorescence analysis of neuromuscular junctions (NMJs), and assessment of skeletal muscle physiology, contractile properties, and integrity were conducted. Results Castration led to SC activation, however this did not result in a decline in SC function or skeletal muscle regenerative capacity. Surprisingly, castration induced SC-dependent maintenance of young skeletal muscle. The functional dependence of skeletal muscles on SCs in young castrated mice was demonstrated by an increase in SC-derived-cell fusion within skeletal muscle fibers. SC depletion was associated with further atrophy and functional decline, as well as the induction of partial innervation and the loss of NMJ-associated myonuclei in skeletal muscles from castrated mice. Conclusion The maintenance of skeletal muscles in young castrated mice relies on the cellular contributions of SCs. Considering the well-described age-related decline in SCs, the results in this study highlight the need to devise strategies that promote SC maintenance and activity to attenuate or reverse the progression of sarcopenia in elderly androgen-deprived individuals.

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Cancer cachexia and its pathophysiology: links with sarcopenia, anorexia and asthenia

Silva

Santos

Silva

et al. 2020

J cachexia sarcopenia muscle

238

191

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Cancer cachexia is a multifactorial syndrome characterized by a progressive loss of skeletal muscle mass, along with adipose tissue wasting, systemic inflammation and other metabolic abnormalities leading to functional impairment. Cancer cachexia has long been recognized as a direct cause of complications in cancer patients, reducing quality of life and worsening disease outcomes. Some related conditions, like sarcopenia (age‐related muscle wasting), anorexia (appetite loss) and asthenia (reduced muscular strength and fatigue), share some key features with cancer cachexia, such as weakness and systemic inflammation. Understanding the interplay and the differences between these conditions is critical to advance basic and translational research in this field, improving the accuracy of diagnosis and contributing to finally achieve effective therapies for affected patients.

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Smad4 restricts differentiation to promote expansion of satellite cell derived progenitors during skeletal muscle regeneration

Cited by 33 publications

References 47 publications

Regulation and phylogeny of skeletal muscle regeneration

Regulation and phylogeny of skeletal muscle regeneration

Castration induces satellite cell activation that contributes to skeletal muscle maintenance

Cancer cachexia and its pathophysiology: links with sarcopenia, anorexia and asthenia

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