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Your search keyword '"Peck, Bailey D."' showing total 23 results
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23 results on '"Peck, Bailey D."'

10. Mechanical overload‐induced muscle‐derived extracellular vesicles promote adipose tissue lipolysis

Author

Vechetti, Ivan J., primary, Peck, Bailey D., additional, Wen, Yuan, additional, Walton, R. Grace, additional, Valentino, Taylor R., additional, Alimov, Alexander P., additional, Dungan, Cory M., additional, Van Pelt, Douglas W., additional, von Walden, Ferdinand, additional, Alkner, Björn, additional, Peterson, Charlotte A., additional, and McCarthy, John J., additional

Published
2021
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11. Muscle transcriptional networks linked to resistance exercise training hypertrophic response heterogeneity

Author

Lavin, Kaleen M., primary, Bell, Margaret B., additional, McAdam, Jeremy S., additional, Peck, Bailey D., additional, Walton, R. Grace, additional, Windham, Samuel T., additional, Tuggle, S. Craig, additional, Long, Douglas E., additional, Kern, Philip A., additional, Peterson, Charlotte A., additional, and Bamman, Marcas M., additional

Published
2021
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13. Satellite Cell Depletion Disrupts Transcriptional Coordination and Muscle Adaptation to Exercise

Author

Englund, Davis A, primary, Figueiredo, Vandré C, additional, Dungan, Cory M, additional, Murach, Kevin A, additional, Peck, Bailey D, additional, Petrosino, Jennifer M, additional, Brightwell, Camille R, additional, Dupont, Alec M, additional, Neal, Ally C, additional, Fry, Christopher S, additional, Accornero, Federica, additional, McCarthy, John J, additional, and Peterson, Charlotte A, additional

Published
2020
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14. TRANSCRIPTOMIC AND CELLULAR RESPONSE TO MECHANICAL OVERLOAD AND THE UNDERLYING ROLE OF MACROPHAGES IN EXTRACELLULAR MATRIX REMODELING

Author

Peck, Bailey D.

Subjects
FOS: Health sciences
Abstract

The extracellular matrix (ECM) in skeletal muscle plays an integral role in tissue development, structural support, and force transmission. Upon mechanical loading, including resistance exercise, which alter muscle fiber contractile activity, size, orientation and connectivity, remodeling processes must occur that involve both ECM deposition and degradation. ECM remodeling involves many cell types in muscle, but the focus of our research was directed towards macrophages, which participate in the early immune response to damage and loading. We have consistently demonstrated a significant increase in skeletal muscle macrophage abundance using pan macrophage markers (CD11b/CD68) and anti-inflammatory markers (CD206/CD163) following exercise training in both middle aged and older adults. We report that with 14-weeks of progressive resistance exercise training (PRT) in older adults (>65 years of age), genes involved in ECM remodeling, including MMP14, a master regulator of ECM turnover, were the most upregulated, differentially expressed genes among those identified by RNA-sequencing in muscle biopsies. Following an acute bout of resistance exercise in humans and mechanical overload in mouse, single cell RNA-sequencing indicated that muscle macrophages accumulate MMP14 mRNA. In vitro, we identified leukemia inhibitory factor (LIF), secreted by electrically-stimulate primary human myotubes, as a contributor to upregulation of MMP14 expression in macrophages. The data presented identify a novel mechanism by which skeletal muscle and macrophages interact to promote ECM remodeling in response to mechanical overload., © 2020 Bailey D. Peck

Published
2020
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18. Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults: A randomized, double‐blind, placebo‐controlled, multicenter trial: The MASTERS trial

Author

Walton, R. Grace, primary, Dungan, Cory M., additional, Long, Douglas E., additional, Tuggle, S. Craig, additional, Kosmac, Kate, additional, Peck, Bailey D., additional, Bush, Heather M., additional, Villasante Tezanos, Alejandro G., additional, McGwin, Gerald, additional, Windham, Samuel T., additional, Ovalle, Fernando, additional, Bamman, Marcas M., additional, Kern, Philip A., additional, and Peterson, Charlotte A., additional

Published
2019
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22. Resident muscle stem cells are not required for testosterone-induced skeletal muscle hypertrophy.

Author

Englund DA, Peck BD, Murach KA, Neal AC, Caldwell HA, McCarthy JJ, Peterson CA, and Dupont-Versteegden EE

Subjects
Animals, Disease Models, Animal, Hypertrophy chemically induced, Mice, Transgenic, Muscle Fibers, Skeletal physiology, PAX7 Transcription Factor genetics, Satellite Cells, Skeletal Muscle physiology, Muscle Fibers, Skeletal drug effects, Satellite Cells, Skeletal Muscle drug effects, Stem Cells drug effects, Testosterone pharmacology
Abstract

It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this hypothesis, we utilized the Pax7-DTA mouse model to deplete satellite cells in skeletal muscle followed by testosterone administration. Pax7-DTA mice (6 mo of age) were treated for 5 days with either vehicle [satellite cell replete (SC+)] or tamoxifen [satellite cell depleted (SC-)]. Following a washout period, a testosterone propionate or sham pellet was implanted for 21 days. Testosterone administration caused a significant increase in muscle fiber cross-sectional area in SC+ and SC- mice in both oxidative (soleus) and glycolytic (plantaris and extensor digitorum longus) muscles. In SC+ mice treated with testosterone, there was a significant increase in both satellite cell abundance and myonuclei that was completely absent in testosterone-treated SC- mice. These findings provide direct evidence that testosterone-induced muscle fiber hypertrophy does not require an increase in satellite cell abundance or myonuclear accretion.Listen to a podcast about this Rapid Report with senior author E. E. Dupont-Versteegden (https://ajpcell.podbean.com/e/podcast-on-paper-that-shows-testosterone-induced-skeletal-muscle-hypertrophy-does-not-need-muscle-stem-cells/).

Published
2019
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23. Immunohistochemical Identification of Human Skeletal Muscle Macrophages.

Author

Kosmac K, Peck BD, Walton RG, Mula J, Kern PA, Bamman MM, Dennis RA, Jacobs CA, Lattermann C, Johnson DL, and Peterson CA

Abstract

Macrophages have well-characterized roles in skeletal muscle repair and regeneration. Relatively little is known regarding the role of resident macrophages in skeletal muscle homeostasis, extracellular matrix remodeling, growth, metabolism and adaptation to various stimuli including exercise and training. Despite speculation into macrophage contributions during these processes, studies characterizing macrophages in non-injured muscle are limited and methods used to identify macrophages vary. A standardized method for the identification of human resident skeletal muscle macrophages will aide in the characterization of these immune cells and allow for the comparison of results across studies. Here, we present an immunohistochemistry (IHC) protocol, validated by flow cytometry, to distinctly identify resident human skeletal muscle macrophage populations. We show that CD11b and CD206 double IHC effectively identifies macrophages in human skeletal muscle. Furthermore, the majority of macrophages in non-injured human skeletal muscle show a 'mixed' M1/M2 phenotype, expressing CD11b, CD14, CD68, CD86 and CD206. A relatively small population of CD11b+/CD206- macrophages are present in resting skeletal muscle. Changes in the relative abundance of this population may reflect important changes in the skeletal muscle environment. CD11b and CD206 IHC in muscle also reveals distinct morphological features of macrophages that may be related to the functional status of these cells.

Published
2018
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