Expression of thyroid hormone receptors A and B in developing rat tissues: Evidence for extensive posttranscriptional regulation

Abstract

The perinatal changes in the pattern of expression of the thyroid hormone receptor (TR) isoforms TRα1 TRα 2, TRβ1, and TRβ2 were investigated using in situ hybridization and immunohistochemistry, and RT-PCR and western blotting as visualization and quantification techniques respectively. In liver, lung, and kidney, TRα mRNA was expressed in the stromal and TRβ mRNA in the parenchymal component of the tissues. When compared with liver, TRα mRNA concentrations were tenfold higher in lung, kidney, and intestine, and 100-fold higher in brain, with TRα2 mRNA concentrations exceeding those of TRα1 5- to 10-fold. Tissue TRβ1 mRNA concentrations were similar in liver, lung, and brain, and 3- to 5-fold higher in kidney and intestine. None of the TRβ2 mRNA could be detected outside the pituitary. Tissue TRα2 and TRβ1 protein levels reached adult levels at 5 days before birth, whereas TRα1 protein peaked after birth. Because of the distinct time-course of thyroid hormone-binding receptors TRα1 and TRβ1, we speculate that an initiating, TRβ1-mediated signaling from the parenchyma is followed by a TRα1-mediated response in the stroma. When compared with organs with a complementary parenchymal-stromal expression pattern, organs with extensive cellular co-expression of TRα and TRβ (brain and intestinal epithelium) were characterized by a very low TRα protein: mRNA ratio, implying a low translational efficiency of TR mRNA or a high turnover of TR protein. The data indicate that the TR-dependent regulatory cascades are controlled differently in organs with a complementary tissue expression pattern and in those with cellular co-expression of the TRα and TRβ genes. © 2007 Society for Endocrinology.