Senescence and Apoptosis in Aging Skeletal Muscle
Year: 2017
Type: conference-abstract
Abstract: In mitotic cells, senescence and apoptosis occur in response to certain stressors (e.g., aging). However, in post-mitotic cells, such as multinucleated skeletal muscle myofibers the extent to which cellular senescence and apoptosis occurs is largely unknown. Therefore, the purpose of this study was to explore the role of senescence and apoptosis as drivers of age-associated sarcopenia. We hypothesized that biomarkers of senescence and apoptosis would increase in aging skeletal myofibers and that these changes would be associated with sarcopenia. To identify biomarkers of senescence and apoptosis, the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles were examined from adult (<12 months, N=11) and elderly (>28 months, N=11) male C57BL/6 mice. The EDL was used to assess ex vivo whole muscle physiology while the TA was used to determine protein content (p53, p21, p16, caspase 3, and IL-6) and presence of SA ß-gal and Tunnel via histological staining. Muscle wet weight and absolute force production were significantly reduced in the elderly mice. Aging significantly increased p21, IL-6, and caspase 3 content; however, did not appear to impact p53 nor p16 expression. Myofibers of elderly mice had an increase of apoptotic myonuclei, but only presented a small percentage of SA ß-gal. Taken together, biomarkers of cellular senescence and apoptosis are present in muscle of elderly mice. Because p21, IL-6, caspase 3, and apoptotic cells were increased in the elderly muscle it is possible that these pathways contribute to sarcopenia.
Source: Innovation in Aging
Authors: D. Kwak, C.W. Baumann, L.V. Thompson
Institutions: Boston University, University of Minnesota
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,977
OpenAlex ID: W2730477286