Satellite cells function as skeletal muscle stem cells to support postnatal 
muscle growth and regeneration following injury or disease. There is great 
promise for the improvement of muscle performance in livestock and for the 
therapy of muscle pathologies in humans by the targeting of myostatin (MSTN) in 
this cell population. Human diet contains many histone deacetylase (HDAC) 
inhibitors, such as the bioactive component sulforaphane (SFN), whose epigenetic 
effects on MSTN gene in satellite cells are unknown. Therefore, we aimed to 
investigate the epigenetic influences of SFN on the MSTN gene in satellite 
cells. The present work provides the first evidence, which is distinct from the 
effects of trichostatin A (TSA), that SFN supplementation in vitro not only acts 
as a HDAC inhibitor but also as a DNA methyltransferase (DNMT) inhibitor in 
porcine satellite cells. Compared with TSA and 5-aza-2'-deoxycytidine 
(5-aza-dC), SFN treatment significantly represses MSTN expression, accompanied 
by strongly attenuated expression of negative feedback inhibitors of the MSTN 
signaling pathway. miRNAs targeting MSTN are not implicated in 
posttranscriptional regulation of MSTN. Nevertheless, a weakly enriched myoblast 
determination (MyoD) protein associated with diminished histone acetylation in 
the MyoD binding site located in the MSTN promoter region may contribute to the 
transcriptional repression of MSTN by SFN. These findings reveal a new mode of 
epigenetic repression of MSTN by the bioactive compound SFN. This novel 
pharmacological, biological activity of SFN in satellite cells may thus allow 
for the development of novel approaches to weaken the MSTN signaling pathway, 
both for therapies of human skeletal muscle disorders and for livestock 
production improvement.