TY - JOUR
T1 - Fbxw7β is an inducing mediator of dexamethasone-induced skeletal muscle atrophy in vivo with the axis of Fbxw7β-myogenin–atrogenes
AU - Shin, Kyungshin
AU - Ko, Young Gyu
AU - Jeong, Jaemin
AU - Kwon, Heechung
N1 - Funding Information:
Acknowledgements This study was supported by a grant of the Korea Institute of Radiological and Medical Sciences (KIRAMS), funded by Ministry of Science and ICT (MSIT), Republic of Korea (1711042677; 1711045548; 1711045553; 1711045555/50534-2017) and by the Radiation Medicine Research Program through the National Research Foundation of Korea (NRF) (NRF-2017M2A2A7A01070970/50043-2017), funded by the Ministry of Science and ICT (MSIT), Republic of Korea.
Publisher Copyright:
© 2018, Springer Science+Business Media B.V., part of Springer Nature.
PY - 2018/8/1
Y1 - 2018/8/1
N2 - Muscle atrophy is induced by several pathways, e.g., it can be attributed to inherited cachectic symptoms, genetic disorders, sarcopenia, or chronic side effects of treatments. However, the underlying regulatory mechanisms that contribute to muscle atrophy have not been fully elucidated. In this study, we evaluated the role of Fbxw7β, an ubiquitin E3 ligase, in a dexamethasone-induced muscle atrophy model. In this model, endogenous Fbxw7β was up-regulated; furthermore, the Fbxw7β-myogenin–atrogene axis was upregulated, supporting our previous results linking Fbxw7β to muscle atrophy in vitro. Also, muscle atrophy was associated with the Fbxw7β-myogenin–atrogene axis and the down-regulation of Dach2, a repressor of myogenin. Taken together, these results suggest that the ubiquitin E3 ligase Fbxw7β and the Fbxw7β-myogenin–atrogene axis have important roles in a dexamethasone-induced muscle atrophy model in vivo and in vitro. Additionally, the Fbxw7β-Dach2-myogenin–atrogene axis is a potential mechanism underlying muscle atrophy in cases of abnormal Fbxw7β expression-induced muscle atrophy or myogenic degenerative disease.
AB - Muscle atrophy is induced by several pathways, e.g., it can be attributed to inherited cachectic symptoms, genetic disorders, sarcopenia, or chronic side effects of treatments. However, the underlying regulatory mechanisms that contribute to muscle atrophy have not been fully elucidated. In this study, we evaluated the role of Fbxw7β, an ubiquitin E3 ligase, in a dexamethasone-induced muscle atrophy model. In this model, endogenous Fbxw7β was up-regulated; furthermore, the Fbxw7β-myogenin–atrogene axis was upregulated, supporting our previous results linking Fbxw7β to muscle atrophy in vitro. Also, muscle atrophy was associated with the Fbxw7β-myogenin–atrogene axis and the down-regulation of Dach2, a repressor of myogenin. Taken together, these results suggest that the ubiquitin E3 ligase Fbxw7β and the Fbxw7β-myogenin–atrogene axis have important roles in a dexamethasone-induced muscle atrophy model in vivo and in vitro. Additionally, the Fbxw7β-Dach2-myogenin–atrogene axis is a potential mechanism underlying muscle atrophy in cases of abnormal Fbxw7β expression-induced muscle atrophy or myogenic degenerative disease.
KW - Atrogenes
KW - Dach2
KW - Dexamethasone
KW - Fbxw7β
KW - Myogenin
KW - Skeletal muscle atrophy
UR - http://www.scopus.com/inward/record.url?scp=85045633864&partnerID=8YFLogxK
U2 - 10.1007/s11033-018-4185-9
DO - 10.1007/s11033-018-4185-9
M3 - Article
C2 - 29671242
AN - SCOPUS:85045633864
VL - 45
SP - 625
EP - 631
JO - Molecular Biology Reports
JF - Molecular Biology Reports
SN - 0301-4851
IS - 4
ER -