Methylprednisolone increases dystrophin levels by inhibiting myotube death during myogenesis of normal human muscle in vitro.

The glucocorticoid methylprednisolone (Mepd) increased dystrophin and myosin heavy chain levels in differentiated cultures of cloned human myoblasts. Mepd increased the number of myotubes per area by preventing myotube death and detachment during myogenesis in vitro. Myotube death was the result of an endogenous process initiated early during myoblast fusion. It occurred between days 4 and 5 of differentiation (3 days after its initiation) and was inhibited by cycloheximide, indicating that a programmed death mechanism may be involved. Inhibition of myotube death accounted for the increased levels of muscle-specific proteins; the amount of dystrophin per myonucleus was the same with or without Mepd treatment. These effects of glucocorticoids on primary muscle cultures may bear on the recent observation that prednisone transiently enhances muscle function in Duchenne muscular dystrophy.