Hormonal regulation of myoblast proliferation and myotube production in vivo: Influence of prostaglandins

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Abstract
The study of myoblast proliferation and fusion to form myotubes in vivo has centered around the role of the innervating motoneurones. Hormonal factors such as prostaglandin E1 (PGE1) are important during in vitro myogenesis, but their role in vivo has yet to be elucidated. In vitro, PGE1 appears to switch myoblast from a mitotic to a fusion mode. Consistent with this hypothesis, administration of PGE1 to chicken embryos decreased the number of myonuclei incorporated into their muscles. The effect of inhibitors of prostaglandin synthesis (aspirin and indomethacin) on in vivo myogenesis was not, however, as expected. Both drugs decreased the number of myonuclei incorporated into the muscles of treated embryos, which is the opposite of what would have been expected if they were enabling myoblasts to undergo additional divisions by delaying their onset from the mitotic cycle. The simplest explanation of this observation is that the effect of aspirin and indomethacin is mediated by a prostaglandin other than E1, or by a systemic factor whose levels are regulated by a prostaglandin. The maximum extent of the reduction caused by PGE1 and the inhibitors of prostaglandin synthesis was only 25–30%, suggesting that only a subpopulation of myoblasts is effected by these drugs. The number of myotubes formed in the treated embryos closely paralleled the total number of myonuclei, indicating that the number of myoblasts fusing to form a myotube is constant even when the total number of available myoblasts is diminished.