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Deficiency of Bax promotes compensatory muscle hypertrophy as induced by denervation of agonists
Author(s) -
Siu Parco M,
Alway Stephen E
Publication year - 2010
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.24.1_supplement.989.15
Subject(s) - plantaris muscle , denervation , muscle hypertrophy , medicine , endocrinology , hindlimb , soleus muscle , apoptosis , gastrocnemius muscle , chemistry , compensatory hypertrophy , anatomy , biology , skeletal muscle , biochemistry
The purpose of the present study was to determine the effect of interference of apoptosis on muscle hypertrophy. We tested the hypothesis that the extent of muscle hypertrophy is enhanced in muscle of mice that are deficient of the pro‐apoptotic Bax gene. Experiments were conducted on adult wild‐type mice (n=8) and Bax gene‐deficient mice (n=6). The medial and lateral branches of tibial nerve that innervate the plantar flexor gastrocnemius and soleus were transected close to their neuromuscular junction. This experimental procedure left the contractile activities of plantar flexor plantaris intact which was induced for compensatory muscle hypertrophy. The denervation procedure was performed in right hind limb and sham procedure was performed in left hind limb, which served as the intra‐animal contralateral control. After 14 days of soleus and gastrocnemius denervation, no significant increase in plantaris muscle mass was found in wild‐type mice whereas significant compensatory hypertrophy was evident in plantaris of Bax −/− mice in which the plantaris muscle mass was significantly increased by 24% (P<.05) in Bax −/− mice. The cytoplasmic content of cytochrome c was significantly reduced by 32% (P<.05) in plantaris of Bax −/− mice with hypertrophy whereas no change was observed in that of wild‐type mice. Hydrogen peroxide content in muscle tissue was measured by fluorimetric assay but no changes were found in plantaris of both Bax −/− and wild‐type mice. These data demonstrated the enhancement of compensatory muscle hypertrophy as induced by denervation of agonists is accompanied by suppressed pro‐apoptotic signaling in skeletal muscle that is deficient of Bax. The present findings suggest that apoptotic signaling is involved in the adaptation of muscle hypertrophy.