Population of muscle satellite cells in relation to age and mitotic activity

Allbrook, David; Han, M.F.; Hellmuth, A.E.

doi:10.1080/00313027109073739

Cited by 146 publications

(53 citation statements)

References 7 publications

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“…Satellite cells account for ~30-35% of the sublaminal nuclei of myofibres in early postnatal mouse muscle, but this proportion falls over time and, by adulthood, only 1-4% of nuclei belong to satellite cells (Allbrook et al, 1971;Hellmuth and Allbrook, 1971;Schultz, 1974). By contrast, the number of myonuclei in muscle increases during postnatal growth (Enesco and Puddy, 1964).…”

Section: Satellite Cells In Growing Postnatal Musclementioning

confidence: 99%

All muscle satellite cells are equal, but are some more equal than others?

Zammit

2008

Journal of Cell Science

182

160

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Skeletal muscle is an accessible adult stem-cell model in which differentiated myofibres are maintained and repaired by a selfrenewing stem-cell compartment. These resident stem cells, which are known as satellite cells, lie on the surface of the muscle fibre, between the plasmalemma and overlying basal lamina. Although they are normally mitotically quiescent in adult muscle, satellite cells can be activated when needed to generate myoblasts, which eventually differentiate to provide new myonuclei for the homeostasis, hypertrophy and repair of muscle fibres, or fuse together to form new myofibres for regeneration. Satellite cells also self-renew in order to maintain a viable stem-cell pool that is able to respond to repeated demand. The study of the control of self-renewal has led to the idea that the satellite-cell pool might be heterogeneous: that is it might contain both self-renewing satellite 'stem' cells and myogenic precursors with limited replicative potential in the same anatomical location. The regulatory circuits that control satellite-cell self-renewal are beginning to be deciphered, with Pax7, and Notch and Wnt signalling being clearly implicated. This Commentary seeks to integrate these interesting new findings into the wider context of satellite-cell biology, and to highlight some of the many outstanding questions. SummaryAll muscle satellite cells are equal, but are some more equal than others? Peter S. ZammitKingʼs College London, Randall Division of Cell and Molecular Biophysics, New Huntʼs House, Guyʼs Campus, London SE1 1UL, UK Author for correspondence (e-mail: peter.zammit@kcl.ac.uk) Accepted 24 July 2008 Journal of Cell Science 121, 2975-2982 Published by The Company of Biologists 2008Biologists doi:10.1242 Journal of Cell Science 2976 DNA replication during S phase by using tritiated thymidine suggested that labelled satellite cells give rise to myonuclei following cell division (Moss and Leblond, 1970); this was later confirmed by many other studies. Importantly, the tracking of DNA replication also indicated that satellite-cell divisions could be asymmetric in growing muscle and give rise to both myonuclei and satellite cells, which suggests that satellite cells self-renew (Moss and Leblond, 1971). The satellite-cell population in growing muscle can be separated into two groups: a fast-dividing population that undergoes limited replication before differentiating, and a slow-dividing population that might return to G0 between cycles and give rise to the fast-dividing population (Schultz, 1996).Together, these data suggest that, during the early postnatal period, fast-dividing satellite cells initially undergo asymmetric divisions to produce both myonuclei for muscle growth and satellite cells, but later undergo symmetric divisions, so that few of the fastdividing cells remain as satellite cells in adult muscle. The bulk of the satellite cells that exist in adults, therefore, presumably derives from the slow-dividing population. This raises the question of whether most satellite ce...

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Section: Satellite Cells In Growing Postnatal Musclementioning

confidence: 99%

All muscle satellite cells are equal, but are some more equal than others?

Zammit

2008

Journal of Cell Science

182

160

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“…Here we show the percentage of centrally located myofiber nuclei because it is one the most robust pathology measures in mdx muscles. As normal myofibers mature, nuclei migrate out to the periphery of the myofiber, such that fewer than 5% remain in a central position [20][21][22][23]. However, if dystrophin-lacking muscles are damaged and undergo regeneration in the adult mouse, nuclei within the regenerated myofiber remain in a central position for most of the life of the animal.…”

Section: Length Of Inhibition Of Muscular Dystrophy By Galgt2mentioning

confidence: 99%

Postnatal overexpression of the CT GalNAc transferase inhibits muscular dystrophy in mdx mice without altering muscle growth or neuromuscular development: Evidence for a utrophin-independent mechanism

Camboni

Martin

2007

Neuromuscular Disorders

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Overexpression of the cytotoxic T cell (CT) GalNAc transferase (Galgt2) in the skeletal muscles of transgenic mdx mice inhibits the development of muscular dystrophy. The profound effect of Galgt2 on muscular dystrophy in transgenic mice, where overexpression is begins from embryonic stages, is complicated by its additional effects on muscle growth and neuromuscular structure. Here, we use Adeno-associated virus (AAV) to show that overexpression of Galgt2 in skeletal myofibers in the early postnatal period is equally effective in inhibiting muscular dystrophy, but that it does so without altering muscle growth or neuromuscular structure. Unlike embryonic overexpression, postnatal overexpression of Galgt2 did not reproducibly increase the expression of utrophin, synaptic laminins, or dystrophin-associated glycoproteins along infected myofibers. Moreover, Galgt2 overexpression inhibited muscular dystrophy to the same extent in utrophin-deficient mdx muscles as it did in utrophin-expressing mdx muscles. Thus, Galgt2 is a molecular target for therapy in DMD that can be utilized in a manner that separates its clinical benefit from its effects on development, and its clinical benefit is distinct from that achieved by utrophin.

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“…(143) Moreover, differences in satellite cell number and proliferative capacity have been noted in mouse and rat satellite cells isolated from the skeletal muscle of 3-monthold compared to 7-month-old rodents. (140,144,145) Taken together, these indings indicate that age-related changes in satellite cell self-renewal, proliferative and differentiation capacity are likely due to both extrinsic alterations in the microenvironment and intrinsic alterations in cellautonomous regulatory mechanisms. (146) Aged skeletal muscle undergoes a progressive reduction in the cross-sectional area of muscle ibers (147), selective loss of fast glycolytic ibers (148), and increase in muscle connective tissue (149).…”

Section: Indones Biomed J 2015; 7(2): 73-86mentioning

confidence: 82%

“…(126,137,138) Notably, as an organism ages, a decrease in regenerative capacity is concomitant with a decrease in satellite cell numbers. (139,140) The reduced regenerative potential observed in aging skeletal muscle is attributed primarily to changes in the muscle niche. Soluble ligands from the Notch, Wnt and transforming growth factor (TGF)-β signaling pathways are deregulated both systemically and within the satellite cell niche.…”

Section: Indones Biomed J 2015; 7(2): 73-86mentioning

confidence: 99%

Molecular Regulation and Rejuvenation of Muscle Stem (Satellite) Cell Aging

2015

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BACKGROUND: Age-related muscle loss leads to lack of muscle strength, resulting in reduced posture and mobility and an increased risk of falls, all of which contribute to a decrease in quality of life. Skeletal muscle regeneration is a complex process, which is not yet completely understood.CONTENT: Skeletal muscle undergoes a progressive agerelated loss in mass and function. Preservation of muscle mass depends in part on satellite cells, the resident stem cells of skeletal muscle. Reduced satellite cell function may contribute to the age-associated decrease in muscle mass. Recent studies have delineated that the aging process in organ stem cells is largely caused by age-speciic changes in the differentiated niches, and that regenerative outcomes often depend on the age of the niche, rather than on stem cell age. It is likely that epigenetic states will be better deine such key satellite cell features as prolonged quiescence and lineage idelity. It is also likely that DNA and histone modiications will underlie many of the changes in aged satellite cells that account for age-related declines in functionality and rejuvenation through exposure to the systemic environment. SUMMARY:Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Decreased muscle stem cell function in aging has long been shown to depend on altered environmental cues, whereas the contribution of intrinsic mechanisms remained less clear. Signals in the aged niche were shown to cause permanent defects in the ability of satellite cells to return to quiescence, ultimately also impairing the maintenance of self-renewing satellite cells. Therefore, only anti-aging strategies taking both factors, the stem cell niche and the stem cells per se, into consideration may ultimately be successful.

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Population of muscle satellite cells in relation to age and mitotic activity

Cited by 146 publications

References 7 publications

All muscle satellite cells are equal, but are some more equal than others?

All muscle satellite cells are equal, but are some more equal than others?

Postnatal overexpression of the CT GalNAc transferase inhibits muscular dystrophy in mdx mice without altering muscle growth or neuromuscular development: Evidence for a utrophin-independent mechanism

Molecular Regulation and Rejuvenation of Muscle Stem (Satellite) Cell Aging

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