Although thyroid hormone has been known for many years to be a potent regul
ator of skeletal maturation in vivo, it has not definitively been determine
d whether this effect is a result of a direct or indirect action of the hor
mone, Previous in vivo studies have suggested that thyroid hormone may stim
ulate longitudinal bone growth by increasing the secretion of growth hormon
e; however, growth hormone alone is unable to stimulate cartilage maturatio
n. There are also indications that thyroid hormone is able to act directly
on growth plate chondrocytes through growth hormone-independent mechanisms.
In this study,we demonstrate that rat growth plate chondrocytes in vivo ex
press genes encoding three of the four isoforms of the thyroid hormone rece
ptors described to date, but the corresponding protein can only be detected
for the TR alpha 1 and TR beta 1 isoforms of the receptor. As has been not
ed in other tissues, there is generally poor correlation between the mRNA l
evels for each isoform and the relative amount of corresponding protein as
measured by immunoblotting, suggesting the possibility that receptor expres
sion may be regulated by post-transcriptional mechanisms.