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2. Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia

Author

Fry, Christopher S., Lee, Jonah D., Mula, Jyothi, Kirby, Tyler J., Jackson, Janna R., Liu, Fujun, Yang, Lin, Mendias, Christopher L., Dupont-Versteegden, Esther E., McCarthy, John J., and Peterson, Charlotte A.

Subjects
Sarcopenia -- Analysis -- Development and progression -- Genetic aspects -- Research, Regeneration (Biology) -- Physiological aspects -- Genetic aspects -- Research, Muscles -- Analysis -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

A key determinant of geriatric frailty is sarcopenia, the age-associated loss of skeletal muscle mass and strength (1,2). Although the etiology of sarcopenia is unknown, the correlation during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells, and impaired muscle regenerative capacity has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia (3,4). We tested this hypothesis in male sedentary mice by experimentally depleting satellite cells in young adult animals to a degree sufficient to impair regeneration throughout the rest of their lives. A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis. These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis., Recent estimates indicate that up to one-third of elderly people suffer from frailty, characterized by a common set of symptoms including loss of muscle strength, increased fatigability, modest levels of [...]

Published
2015

4. Intrinsic muscle clock is necessary for musculoskeletal health

Author

Schroder, Elizabeth A., Harfmann, Brianna D., Zhang, Xiping, Srikuea, Ratchakrit, England, Jonathan H., Hodge, Brian A., Wen, Yuan, Riley, Lance A., Yu, Qi, Christie, Alexander, Smith, Jeffrey D., Seward, Tanya, Wolf Horrell, Erin M., Mula, Jyothi, Peterson, Charlotte A., Butterfield, Timothy A., and Esser, Karyn A.

Published
2015
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6. Mss51 deletion enhances muscle metabolism and glucose homeostasis in mice

Author

Rovira Gonzalez, Yazmin I., primary, Moyer, Adam L., additional, LeTexier, Nicolas J., additional, Bratti, August D., additional, Feng, Siyuan, additional, Sun, Congshan, additional, Liu, Ting, additional, Mula, Jyothi, additional, Jha, Pankhuri, additional, Iyer, Shama R., additional, Lovering, Richard, additional, O’Rourke, Brian, additional, Noh, Hye Lim, additional, Suk, Sujin, additional, Kim, Jason K., additional, Essien Umanah, George K., additional, and Wagner, Kathryn R., additional

Published
2019
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8. Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity but does not contribute to sarcopenia

Author

Fry, Christopher S., Lee, Jonah D., Mula, Jyothi, Kirby, Tyler J., Jackson, Janna R., Liu, Fujun, Yang, Lin, Mendias, Christopher L., Dupont-Versteegden, Esther E., McCarthy, John J., and Peterson, Charlotte A.

Subjects
Aging, Mice, Sarcopenia, Satellite Cells, Skeletal Muscle, Animals, Humans, Regeneration, Muscle, Skeletal, Article
Abstract

A key determinant of geriatric frailty is sarcopenia, the age-associated loss of skeletal muscle mass and strength. Although the etiology of sarcopenia is unknown, the correlation during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells, and impaired muscle regenerative capacity has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia. We tested this hypothesis in male sedentary mice by experimentally depleting satellite cells in young adult animals to a degree sufficient to impair regeneration throughout the rest of their lives. A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis. These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis.

Published
2014

11. Fibre type-specific satellite cell response to aerobic training in sedentary adults

Author

Fry, Christopher S, Noehren, Brian, Mula, Jyothi, Ubele, Margo F, Westgate, Philip M, Kern, Philip A, and Peterson, Charlotte A

Subjects
Male, Myosin Type II, Myosin Type I, Muscle Fibers, Skeletal, Muscle, Humans, Female, musculoskeletal system, Exercise
Abstract

In the present study, we sought to determine the effect of a traditional, 12 week aerobic training protocol on skeletal muscle fibre type distribution and satellite cell content in sedentary subjects. Muscle biopsies were obtained from the vastus lateralis [n = 23 subjects (six male and 17 female); body mass index 30.7 ± 1.2 kg m−2] before and after 12 weeks of aerobic training performed on a cycle ergometer. Immunohistochemical analyses were used to quantify myosin heavy chain (MyHC) isoform expression, cross-sectional area and satellite cell and myonuclear content. Following training, a decrease in MyHC hybrid type IIa/IIx fibre frequency occurred, with a concomitant increase in pure MyHC type IIa fibres. Pretraining fibre type correlated with body mass index, and the change in fibre type following training was associated with improvements in maximal oxygen consumption. Twelve weeks of aerobic training also induced increases in mean cross-sectional area in both MyHC type I and type IIa fibres. Satellite cell content was also increased following training, specifically in MyHC type I fibres, with no change in the number of satellite cells associated with MyHC type II fibres. With the increased satellite cell content following training, an increase in myonuclear number per fibre also occurred in MyHC type I fibres. Hypertrophy of MyHC type II fibres occurred without detectable myonuclear addition, suggesting that the mechanisms underlying growth in fast and slow fibres differ. These data provide intriguing evidence for a fibre type-specific role of satellite cells in muscle adaptation following aerobic training.

Published
2014

12. Concordant but Varied Phenotypes among Duchenne Muscular Dystrophy Patient-Specific Myoblasts Derived using a Human iPSC-Based Model

Author

Choi, In Young, primary, Lim, HoTae, additional, Estrellas, Kenneth, additional, Mula, Jyothi, additional, Cohen, Tatiana V., additional, Zhang, Yuanfan, additional, Donnelly, Christopher J., additional, Richard, Jean-Philippe, additional, Kim, Yong Jun, additional, Kim, Hyesoo, additional, Kazuki, Yasuhiro, additional, Oshimura, Mitsuo, additional, Li, Hongmei Lisa, additional, Hotta, Akitsu, additional, Rothstein, Jeffrey, additional, Maragakis, Nicholas, additional, Wagner, Kathryn R., additional, and Lee, Gabsang, additional

Published
2016
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13. Insulin-resistant subjects have normal angiogenic response to aerobic exercise training in skeletal muscle, but not in adipose tissue

Author

Walton, R. Grace, primary, Finlin, Brian S., additional, Mula, Jyothi, additional, Long, Douglas E., additional, Zhu, Beibei, additional, Fry, Christopher S., additional, Westgate, Philip M., additional, Lee, Jonah D., additional, Bennett, Tamara, additional, Kern, Philip A., additional, and Peterson, Charlotte A., additional

Published
2015
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14. Aged Muscle Demonstrates Fiber-Type Adaptations in Response to Mechanical Overload, in the Absence of Myofiber Hypertrophy, Independent of Satellite Cell Abundance

Author

Lee, Jonah D., primary, Fry, Christopher S., additional, Mula, Jyothi, additional, Kirby, Tyler J., additional, Jackson, Janna R., additional, Liu, Fujun, additional, Yang, Lin, additional, Dupont-Versteegden, Esther E., additional, McCarthy, John J., additional, and Peterson, Charlotte A., additional

Published
2015
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15. Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia

Author

Fry, Christopher S, primary, Lee, Jonah D, additional, Mula, Jyothi, additional, Kirby, Tyler J, additional, Jackson, Janna R, additional, Liu, Fujun, additional, Yang, Lin, additional, Mendias, Christopher L, additional, Dupont-Versteegden, Esther E, additional, McCarthy, John J, additional, and Peterson, Charlotte A, additional

Published
2014
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17. Sarcopenia and hypertrophy in aged skeletal muscle is independent of lifelong muscle stem cell depletion

Author

Lee, Jonah Dan, primary, Mula, Jyothi, additional, Fry, Christopher S, additional, Kirby, Tyler J, additional, Jackson, Janna R, additional, Beggs, Jake A, additional, Campbell, Marilyn S, additional, Kmiec, Tyler E, additional, Dupont‐Versteegden, Esther E, additional, McCarthy, John J, additional, and Peterson, Charlotte A, additional

Published
2013
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20. Satellite Cells are not Prerequisite for Skeletal Muscle Regrowth Following Unloading‐Induced Atrophy

Author

Jackson, Janna Renee, primary, Fry, Chris S., additional, Lee, Jonah D., additional, Mula, Jyothi, additional, Erfani, Rod A., additional, Kirby, Tyler J., additional, Ubele, Margo F., additional, Lawson, Ben A., additional, Campbell, Ken S., additional, McCarthy, John J., additional, Peterson, Charlotte A., additional, and Dupont-Versteegden, Esther E., additional

Published
2012
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22. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle

Author

McCarthy, John J., primary, Mula, Jyothi, additional, Miyazaki, Mitsunori, additional, Erfani, Rod, additional, Garrison, Kelcye, additional, Farooqui, Amreen B., additional, Srikuea, Ratchakrit, additional, Lawson, Benjamin A., additional, Grimes, Barry, additional, Keller, Charles, additional, Van Zant, Gary, additional, Campbell, Kenneth S., additional, Esser, Karyn A., additional, Dupont-Versteegden, Esther E., additional, and Peterson, Charlotte A., additional

Published
2011
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24. Automated fiber-type-specific cross-sectional area assessment and myonuclei counting in skeletal muscle.

Author

Fujun Liu, Fry, Christopher S., Mula, Jyothi, Jackson, Janna R., Lee, Jonah D., Peterson, Charlotte A., and Lin Yang

Subjects
SKELETAL muscle, CHRONIC diseases
Abstract

Skeletal muscle is an exceptionally adaptive tissue that compromises 40% of mammalian body mass. Skeletal muscle functions in locomotion, but also plays important roles in thermogenesis and metabolic homeostasis. Thus characterizing the structural and functional properties of skeletal muscle is important in many facets of biomedical research, ranging from myopathies to rehabilitation sciences to exercise interventions aimed at improving quality of life in the face of chronic disease and aging. In this paper, we focus on automated quantification of three important morphological features of muscle: 1) muscle fiber-type composition; 2) muscle fiber-type-specific cross-sectional area, and 3) myonuclear content and location. We experimentally prove that the proposed automated image analysis approaches for fiber-type-specific assessments and automated myonuclei counting are fast, accurate, and reliable. [ABSTRACT FROM AUTHOR]

Published
2013
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25. Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy.

Author

Jackson JR, Mula J, Kirby TJ, Fry CS, Lee JD, Ubele MF, Campbell KS, McCarthy JJ, Peterson CA, and Dupont-Versteegden EE

Subjects
Animals, Cell Death physiology, Disease Models, Animal, Female, Mice, Mice, Mutant Strains, Muscle, Skeletal injuries, Muscular Atrophy genetics, Weight-Bearing physiology, Muscle, Skeletal cytology, Muscle, Skeletal physiology, Muscular Atrophy pathology, Muscular Atrophy physiopathology, Satellite Cells, Skeletal Muscle cytology, Satellite Cells, Skeletal Muscle physiology
Abstract

Resident muscle stem cells, known as satellite cells, are thought to be the main mediators of skeletal muscle plasticity. Satellite cells are activated, replicate, and fuse into existing muscle fibers in response to both muscle injury and mechanical load. It is generally well-accepted that satellite cells participate in postnatal growth, hypertrophy, and muscle regeneration following injury; however, their role in muscle regrowth following an atrophic stimulus remains equivocal. The current study employed a genetic mouse model (Pax7-DTA) that allowed for the effective depletion of >90% of satellite cells in adult muscle upon the administration of tamoxifen. Vehicle and tamoxifen-treated young adult female mice were either hindlimb suspended for 14 days to induce muscle atrophy or hindlimb suspended for 14 days followed by 14 days of reloading to allow regrowth, or they remained ambulatory for the duration of the experimental protocol. Additionally, 5-bromo-2'-deoxyuridine (BrdU) was added to the drinking water to track cell proliferation. Soleus muscle atrophy, as measured by whole muscle wet weight, fiber cross-sectional area, and single-fiber width, occurred in response to suspension and did not differ between satellite cell-depleted and control muscles. Furthermore, the depletion of satellite cells did not attenuate muscle mass or force recovery during the 14-day reloading period, suggesting that satellite cells are not required for muscle regrowth. Myonuclear number was not altered during either the suspension or the reloading period in soleus muscle fibers from vehicle-treated or satellite cell-depleted animals. Thus, myonuclear domain size was reduced following suspension due to decreased cytoplasmic volume and was completely restored following reloading, independent of the presence of satellite cells. These results provide convincing evidence that satellite cells are not required for muscle regrowth following atrophy and that, instead, the myonuclear domain size changes as myofibers adapt.

Published
2012
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