Effects of Trichostatin A on Mouse Atrophic Soleus Muscles
Muscular atrophy is the result of discontinued use of muscular function for an extended period of time. It causes a reduction in myofiber size, which in turn leads to an overall reduction in whole muscle mass (size). This study involves the use of trichostatin A, a histone deacetylase inhibitor whose primary role is to increase gene transcription by promoting histone hyperacetylation (Minetti, eta/., 2006). Injection of trichostatin A into skeletal muscles increases myofiber size and restoration of muscle performance (Minetti, et a/., 2006). With that known, the effect of trichostatin A on atrophic soleus muscles of healthy mice was studied. Twelve mice were hind limb suspended for 21 days. Upon suspension, 6 of the mice were treated with trichostatin A, while the remaining 6 were untreated and used as a control. Following day 21, the soleus muscles were removed and stored at -80°C. Individually, the muscles were cross-sectioned, stained and analyzed in order to differentiate between the sizes of the fast (type I) and slow (type II) fibers of the treated and untreated muscles. Overall, there was a significant increase in the areas of the muscle fibers that were treated with trichostatin A for 21 days. Trichostatin A can, therefore, be used to effectively increase muscle fiber mass.