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Expression of Active and Latent Myostatin in Overload‐ Induced Hypertrophied Rat Skeletal Muscle
Author(s) -
Affleck Paige A,
Parcell Allen C,
Thomson David M,
Mack Gary W
Publication year - 2013
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.27.1_supplement.lb802
Subject(s) - myostatin , plantaris muscle , muscle hypertrophy , medicine , endocrinology , soleus muscle , skeletal muscle , western blot , biology , biochemistry , gene
Myostatin (GDF‐8) is the chief chalone in skeletal muscle and negatively controls adult skeletal muscle growth. The role of myostatin during overload‐induced hypertrophy of adult muscle is unclear. We tested the hypothesis that overloaded adult rodent skeletal muscle would reduce expression of myostatin. Overload‐induced hypertrophy was induced by unilateral tenotomy of the gastrocnemius tendon in 11 male adult Sprague‐Dawley rats followed by a 2‐week period of compensatory overload of the plantaris and soleus muscles. Western blot analysis was performed to evaluate changes in active and latent complex myostatin protein expression. Significant hypertrophy was noted in the soleus (494 ± 29 vs 405 ± 15 mg, p<0.05) and plantaris (289 ± 12 vs 179 ± 37 mg, p<0.05) muscles following overload. Overloaded plantaris muscle decreased expression of the active myostatin protein by 28.0 ± 6.6 % (p<0.01) while the myostatin precursor decreased slightly (p=0.04). Overloaded soleus muscle decreased expression of the active myostatin protein by 22.5 ± 5.4% (p<0.01) while myostatin precursor was unchanged. Myostatin latent complex expression decreased in the overloaded soleus by 11.4 ± 4.2% (p = 0.03) but was unchanged in the plantaris. These data support the hypothesis that the myostatin‐signaling pathway in overloaded muscles is generally reduced and contributes to muscle hypertrophy.