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- Resistance exercise (2)
- Skeletal muscle (2)
- Aging (1)
- Animals (1)
- Cell growth (1)
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- Cycle training (1)
- Endurance exercise training (1)
- Exercise training (1)
- Exosomes (1)
- Gene Expression Regulation (1)
- Heart Failure (1)
- Heart failure (1)
- Humans (1)
- MicroRNA (1)
- MicroRNAs (1)
- Muscle stem cells (1)
- Muscle, Skeletal (1)
- Myocardium (1)
- P62Ser403 (1)
- Sequestosome1 (1)
- Sestrin (1)
- Skeletal muscle macrophages (1)
Articles 1 - 3 of 3
Full-Text Articles in Musculoskeletal System
Human Skeletal Muscle Macrophages Increase Following Cycle Training And Are Associated With Adaptations That May Facilitate Growth, R. Grace Walton, Kate Kosmac, Jyothi Mula, Christopher S. Fry, Bailey D. Peck, Jason S. Groshong, Brian S. Finlin, Beibei Zhu, Philip A. Kern, Charlotte A. Peterson
Human Skeletal Muscle Macrophages Increase Following Cycle Training And Are Associated With Adaptations That May Facilitate Growth, R. Grace Walton, Kate Kosmac, Jyothi Mula, Christopher S. Fry, Bailey D. Peck, Jason S. Groshong, Brian S. Finlin, Beibei Zhu, Philip A. Kern, Charlotte A. Peterson
Center for Muscle Biology Faculty Publications
Skeletal muscle macrophages participate in repair and regeneration following injury. However, their role in physiological adaptations to exercise is unexplored. We determined whether endurance exercise training (EET) alters macrophage content and characteristics in response to resistance exercise (RE), and whether macrophages are associated with other exercise adaptations. Subjects provided vastus lateralis biopsies before and after one bout of RE, after 12 weeks of EET (cycling), and after a final bout of RE. M2 macrophages (CD11b+/CD206+) did not increase with RE, but increased in response to EET (P < 0.01). Increases in M2 macrophages were positively correlated with fiber hypertrophy (r = 0.49) and satellite cells (r = 0.47). M2c macrophages (CD206+/CD163+) also increased following EET (P < 0.001), and were associated with fiber hypertrophy (r = 0.64). Gene expression was quantified using NanoString. Following EET, the change in M2 macrophages was positively associated with changes in HGF, IGF1, and extracellular matrix genes. EET decreased expression of IL6 (P < 0.05), C/EBPβ (P < 0.01), and MuRF (P < 0.05), and increased expression of IL-4 (P < 0.01), TNFα (P < 0.01) and the TWEAK receptor FN14 (P < 0.05). The change in FN14 gene expression was inversely associated with changes in C/EBPβ (r = −0.58) and MuRF (r = −0.46) following EET. In cultured human myotubes, siRNA inhibition of FN14 increased expression of C/EBPβ (P < 0.05) and MuRF (P < 0.05). Our data suggest that macrophages contribute to the muscle response to EET, potentially including modulation of TWEAK-FN14 signaling.
Acute Resistance Exercise Induces Sestrin2 Phosphorylation And P62 Dephosphorylation In Human Skeletal Muscle, Nina Zeng, Randall F. D'Souza, Vandre C. Figueiredo, James F. Markworth, Llion A. Roberts, Jonathan M. Peake, Cameron J. Mitchell, David Cameron-Smith
Acute Resistance Exercise Induces Sestrin2 Phosphorylation And P62 Dephosphorylation In Human Skeletal Muscle, Nina Zeng, Randall F. D'Souza, Vandre C. Figueiredo, James F. Markworth, Llion A. Roberts, Jonathan M. Peake, Cameron J. Mitchell, David Cameron-Smith
Center for Muscle Biology Faculty Publications
Sestrins (1, 2, 3) are a family of stress-inducible proteins capable of attenuating oxidative stress, regulating metabolism, and stimulating autophagy. Sequestosome1 (p62) is also a stress-inducible multifunctional protein acting as a signaling hub for oxidative stress and selective autophagy. It is unclear whether Sestrin and p62Ser403 are regulated acutely or chronically by resistance exercise (RE) or training (RT) in human skeletal muscle. Therefore, the acute and chronic effects of RE on Sestrin and p62 in human skeletal muscle were examined through two studies. In Study 1, nine active men (22.1 ± 2.2 years) performed a bout of single-leg strength …
Micrornas, Heart Failure, And Aging: Potential Interactions With Skeletal Muscle, Kevin A. Murach, John J. Mccarthy
Micrornas, Heart Failure, And Aging: Potential Interactions With Skeletal Muscle, Kevin A. Murach, John J. Mccarthy
Center for Muscle Biology Faculty Publications
MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression by targeting mRNAs for degradation or translational repression. MiRNAs can be expressed tissue specifically and are altered in response to various physiological conditions. It has recently been shown that miRNAs are released into the circulation, potentially for the purpose of communicating with distant tissues. This manuscript discusses miRNA alterations in cardiac muscle and the circulation during heart failure, a prevalent and costly public health issue. A potential mechanism for how skeletal muscle maladaptations during heart failure could be mediated by myocardium-derived miRNAs released to the circulation is presented. An overview …