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Depressed mitochondrial biogenesis and dynamic remodeling in mouse tibialis anterior and gastrocnemius induced by 4‐week hindlimb unloading
Author(s) -
Liu Jing,
Peng Yunhua,
Cui Zhiwei,
Wu Zhiming,
Qian Airong,
Shang Peng,
Qu Lina,
Li Yinghui,
Liu Jiankang,
Long Jiangang
Publication year - 2012
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1087
Subject(s) - mitochondrial biogenesis , atrophy , hindlimb , muscle atrophy , mitochondrial fission , mitochondrion , tfam , mitochondrial fusion , gastrocnemius muscle , microbiology and biotechnology , biology , medicine , skeletal muscle , endocrinology , chemistry , mitochondrial dna , biochemistry , gene
Mitochondrial dynamics is highly involved in muscle atrophy, the slow twitch muscle as soleus, preferentially affected by hindlimb unloading (HU), was well characterized by mitochondrial dysfunction in biogenesis. However, the fast twitch muscles like tibialis anterior (TA) and gastrocnemius (GAS), which are the most massive parts of the hindlimb muscles, are less elucidated on mitochondrial adaptations responding to HU. To investigate the mitochondrial dynamic responses and the involved molecules mediating atrophy in TA and GAS, we studied a 4‐week HU mouse model. We found GAS was preferentially affected to atrophy by unloading compared with TA. Furthermore, the depressed mitochondrial biogenesis occurred, accounting for mitochondrial loss in GAS by unloading. PGC‐1α, as well as its transcriptional/post‐translational modification regulators, such as p‐CREB, SIRT1, and p‐AMPK, were consistently reduced in response to unloading in GAS. Molecules relevant to autophagy, mitochondrial fusion, and fission, were compromised following unloading both in TA and GAS. These results suggested that TA exhibited resistance to unloading induced muscle atrophy while GAS presented significant mitochondrial loss, which might be due to the mitochondrial biogenesis suppressed by the inactivation of PGC‐1α. However, both in TA and GAS muscles, a similar sedentary mitochondrial dynamics of mitochondrial fusion and fission was induced by unloading though TA exhibited little muscle atrophy. © 2012 IUBMB, IUBMB Life, 64(11): 901–910, 2012

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