Premium
Contribution of Satellite Cells to Skeletal Muscle Proteostasis during Advanced Age and Aerobic Exercise
Author(s) -
Konopka Adam R.,
Ehrlicher Sarah E.,
Baeverstad Kathryn A.,
Reid Justin,
Peelor Fredrick F.,
Confides Amy L.,
DupontVersteegden Esther E.,
Miller Benjamin F.,
Hamilton Karyn L.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1244.2
Subject(s) - proteostasis , skeletal muscle , mitochondrial biogenesis , medicine , endocrinology , extracellular matrix , biology , satellite , aerobic exercise , mitochondrion , microbiology and biotechnology , engineering , aerospace engineering
We have shown that the maintenance of skeletal muscle proteostasis is a shared characteristic in several animal models of slowed aging. Loss of satellite cell activity with advancing age has been correlated to impaired skeletal muscle remodeling however emerging evidence suggests satellite cells may not be requisite in preventing age‐related changes in skeletal muscle. It remains to be determined how satellite cell recruitment influences protein turnover during advanced age and after exercise. We hypothesized that satellite cells will have a minimal contribution to skeletal muscle proteostasis during aging and exercise. To test this hypothesis, at 4 months of age Pax7 CreER ‐DTA mice were treated with vehicle or tamoxifen to deplete satellite cells. The gastrocnemius muscle was harvested from young (7–10 months old) and old (23–24 months old) mice. A subset of mice from both age and treatment groups had access to voluntary running wheels (exercised) for the last two months to provide a stimulus for satellite cell recruitment while the other mice remained ambulatory (non‐exercised). After an intial i.p. bolus, mice received 8% D 2 O in their drinking water during the last 6 weeks of each intervention to assess the integrated synthesis rates of skeletal muscle subcellular fractions and DNA. Skeletal muscle mitochondrial and collagen protein synthesis were lower in aged mice regardless of satellite cell content, which is consistent with the notion of age‐related impairments in mitochondrial biogenesis and extracellular matrix turnover. Compared to vehicle, tamoxifen treatment decreased mitochondrial and collagen synthesis in the young, non‐exercised group. Collagen synthesis remained lower in aged, exercised mice with no influence from satellite cells. Interestingly, when satellite cells were depleted, mitochondrial protein synthesis was elevated in the exercised group. Additional analysis regarding DNA synthesis is forthcoming and warranted to provide context for the novel relationship between satellite cell depletion and augmented mitochondrial biogenesis after exercise. Although the mechanisms linking satellite cell depletion to augmented mitochondrial biogenesis after exercise remain unknown, these data suggest in the absence of satellite cells the energetic stress of exercise may selectively increase mitochondrial protein synthesis. These findings are consistent with our previous studies that indicate energetic stress favors cellular resources to be allocated for maintaining existing cellular structures rather than cell proliferation. Support or Funding Information NIA Grants AG043721 to EEVD and AG042569 to BFM and KLH.