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TFAM Overexpression Prevents Skeletal Muscle Atrophy
Author(s) -
Theilen Nicholas T,
Jeremic Nevena,
Weber Greg,
Tyagi Suresh
Publication year - 2018
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.2018.32.1_supplement.lb492
Subject(s) - tfam , atrophy , medicine , muscle atrophy , endocrinology , skeletal muscle , soleus muscle , sarcopenia , hindlimb , chemistry , mitochondrial biogenesis , biochemistry , gene
The current study aims to investigate if the overexpression of the mitochondrial transcription factor A (TFAM) gene in a transgenic mouse model diminishes soleus and gastrocnemius atrophy occurring with hindlimb suspension (HLS). Additionally, we aim to observe if combining concurrent, treadmill exercise training with TFAM transgenic mice prior to HLS has a synergistic effect in preventing skeletal muscle atrophy. Male transgenic mice aged 12–14 weeks old overexpressing the TFAM gene were assigned to a control (T‐Control), 7‐day HLS (T‐HLS), and 14 exercise sessions prior to 7‐day HLS (T‐Ex+HLS) groups and compared to male C57BL/6 (WT) mice ( all wild‐type data from prior work currently in submission) aged 12–14 weeks old assigned to Control, 7‐day HLS (HLS), 14 exercise sessions prior to 7‐day HLS (Ex+HLS), and 14 exercise sessions (Ex). Results indicate overexpressing TFAM results in a decrease of 8.3% in soleus weight/bodyweight ratio and 2.6% in gastrocnemius weight/bodyweight ratio after HLS compared to losses in wild‐type mice of 27.1% in soleus weight/bodyweight ratio and 21.5% in gastrocnemius weight/bodyweight ratio after HLS. Our data indicates TFAM may play a critical role in protecting skeletal muscle from disuse atrophy and is correlated with increased expression of antioxidants (SOD‐2) and potential redox balance. Our results also indicate combining exercise with TFAM overexpression had no significant increase compared to wild‐type Ex+HLS. TFAM may be a molecule of interest for future pharmaceutical and therapeutic targeting to treat skeletal muscle atrophy. Support or Funding Information The study was supported by NIH Grant HL74185 to SCT. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .