Chronic stress and continually high glucocorticoid levels can induce muscle atrophy. Unfortunately, there is a lack of appropriate animal models for stress-induced muscle atrophy research. Corticotropin releasing factor-overexpressing (CRF-OE) mice are a transgenic model of chronic stress that exhibit increased plasma corticosterone levels and Cushing’s syndrome; however, the skeletal muscle pathology of the CRF-OE mouse has not been well studied. We observed that male, 19-week-old CRF-OE mice had significantly lower skeletal muscle mass, average cross-sectional myofiber area, and total muscle protein content than their wild type (WT) littermates. Muscle function determined by grip strength, wire-hang, and open field tests showed that 19-week-old male CRF-OE mice had impaired physical ability. Additionally, the skeletal muscles of CRF-mice exhibited decreased expression of factors involved in the IGF-1/AKT/mTOR protein synthesis pathway and increased ubiquitin proteasome pathway activity compared to the WT control mice. In conclusion, 19-week-old CRF-OE mice display numerous features of muscle atrophy and thus serve as a model for investigating stress-induced muscle atrophy and interventions to target the deleterious effects of stress on skeletal muscle.
Bibliographical noteFunding Information:
This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) (No. 2019R1A2C2003340).
© 2020 Kang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Agricultural and Biological Sciences(all)