The importance of thyroid hormone in the regulation of in vivo myogeni
c processes is well documented. This hormone stimulates muscle growth
by increasing the fibers number and diameter. In addition, T3 affects
the expression of different myosin isoforms, by a direct transcription
al pathway in cardiac muscle, indirectly in skeletal muscle. Last, acc
ording to the strong effect of this hormone upon mitochondriogenesis a
nd mitochondrial activity, it could be also involved in the processes
of metabolic differentiation. However, the molecular basis of these in
fluences remained largely unknown. Cell culture experiments provide st
rong evidence that T3 stimulates myoblast differentiation, by increasi
ng the rate of myoblast withdrawal from the cell cycle. Recent data su
ggest that in murine myoblasts, MyoD and myo-genin genes transcription
is directly stimulated by T3; however, as a similar phenomenon does n
ot occur in avian myoblasts in which T3 displays a stronger myogenic i
nfluence, such a mechanism is probably not essential. Studies performe
d in avian cells (secondary cultures and QM7 line) indicate that inhib
ition of AP-1 activity is probably a crucial target involved in the T3
myogenic influence.