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Muscle Compression Causes Reduction of Oxidative Phosphorylation (OXPHOS) Subunits and Increase in Autophagy
Author(s) -
Tam Bjorn T.,
Yung Benjamin Y.,
Wong Cesar S.,
Chan Lawrence W.,
Tam Eric W.,
Siu Parco M.
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.742.3
Subject(s) - skeletal muscle , autophagy , oxidative phosphorylation , mitochondrion , microbiology and biotechnology , oxidative stress , chemistry , phosphorylation , downregulation and upregulation , compression (physics) , apoptosis , biochemistry , biology , anatomy , materials science , gene , composite material
Pressure‐induced injury, skeletal muscle apoptosis and nitrosative stress can be induced in skeletal muscle by moderate mechanical compression in our established mouse model. Nonetheless, the effects of mechanical compression on oxidative phosphorylation (OXPHOS) subunits content and autophagic signalling in compressed skeletal muscle are largely unknown. PURPOSE To determine whether mechanical compression decreases the content of OXPHOS subunits and triggers autophagy in skeletal muscle. METHODS A single session of 4‐hour compression with static pressure of 150 mmHg was applied over the right lateral gastrocnemius muscle of mice. Tissues were harvested 48 hours after compression for analysis. RESULTS Our immunoblot data suggest that mechanical compression decreases OXPHOS subunits content. Furthermore, mechanical compression triggers autophagy in compressed skeletal muscle, resulting in increase in LC3‐II protein abundance and decrease in p62 protein abundance. CONCLUSION These results suggest that moderate mechanical compression leads to degradation of mitochondrial complexes which might impair the OXPHOS activity and, hence, the mitochondrial function. The degradation of mitochondrial complexes might possibly be induced by the upregulation of autophagy. Support or Funding Information Supported by The Hong Kong Polytechnic University Research Funds (A‐PH69 and G‐U645) and General Research Fund (PolyU 5632/10M).