Thyroid hormone is essential for normal proliferation and differentiation of 
chondrocytes. Thus, untreated congenital hypothyroidism is marked by severe 
short stature. The monocarboxylate transporter 8 (MCT8) is a highly specific 
transporter for thyroid hormone. The hallmarks of Allan-Herndon-Dudley syndrome, 
caused by MCT8 mutations, are severe psychomotor retardation and elevated T(3) 
levels. However, growth is mostly normal. We therefore hypothesized that growth 
plate chondrocytes use transporters other than MCT8 for thyroid hormone uptake. 
Extensive analysis of thyroid hormone transporter mRNA expression in mouse 
chondrogenic ATDC5 cells revealed that monocarboxylate transporter 10 (Mct10) 
was most abundantly expressed among the transporters known to be highly specific 
for thyroid hormone, namely Mct8, Mct10, and organic anion transporter 1c1. 
Expression levels of Mct10 mRNA diminished with chondrocyte differentiation in 
these cells. Accordingly, Mct10 mRNA was expressed most abundantly in the growth 
plate resting zone chondrocytes in vivo. Small interfering RNA-mediated 
knockdown of Mct10 mRNA in ATDC5 cells decreased [(125)I]T(3) uptake up to 44% 
compared with negative control (P < 0.05). Moreover, silencing Mct10 mRNA 
expression abolished the known effects of T(3), i.e. suppression of 
proliferation and enhancement of differentiation, in ATDC5 cells. These results 
suggest that Mct10 functions as a thyroid hormone transporter in chondrocytes 
and can explain at least in part why Allan-Herndon-Dudley syndrome patients do 
not exhibit significant growth impairment.