RGD Reference Report - Expression of thyroid hormone receptors A and B in developing rat tissues; evidence for extensive posttranscriptional regulation. - Rat Genome Database

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Expression of thyroid hormone receptors A and B in developing rat tissues; evidence for extensive posttranscriptional regulation.

Authors: Keijzer, R  Blommaart, PJ  Labruyere, WT  Vermeulen, JL  Doulabi, BZ  Bakker, O  Tibboel, D  Lamers, WH 
Citation: Keijzer R, etal., J Mol Endocrinol. 2007 May;38(5):523-35.
RGD ID: 2314319
Pubmed: PMID:17496154   (View Abstract at PubMed)
DOI: DOI:10.1677/jme.1.02125   (Journal Full-text)

The perinatal changes in the pattern of expression of the thyroid hormone receptor (TR) isoforms TRalpha (1) TRalpha (2), TRbeta (1), and TRbeta (2) 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, TRalpha mRNA was expressed in the stromal and TRbeta mRNA in the parenchymal component of the tissues. When compared with liver, TRalpha mRNA concentrations were tenfold higher in lung, kidney, and intestine, and 100-fold higher in brain, with TRalpha (2) mRNA concentrations exceeding those of TRalpha (1) 5-to 10-fold. Tissue TRbeta (1) mRNA concentrations were similar in liver, lung, and brain, and 3- to 5-fold higher in kidney and intestine. None of the TRbeta (2) mRNA could be detected outside the pituitary. Tissue TRalpha (2) and TRbeta (1) protein levels reached adult levels at 5 days before birth, whereas TRalpha (1) protein peaked after birth. Because of the distinct time-course of thyroid hormone-binding receptors TRalpha (1) and TRbeta (1), we speculate that an initiating, TRbeta (1)-mediated signaling from the parenchyma is followed by a TRalpha (1)-mediated response in the stroma. When compared with organs with a complementary parenchymal-stromal expression pattern, organs with extensive cellular co-expression of TRalpha and TRbeta (brain and intestinal epithelium) were characterized by a very low TRalpha 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 TRalpha and TRbeta genes.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

Objects Annotated

Genes (Rattus norvegicus)
Thra  (thyroid hormone receptor alpha)
Thra_v1  (thyroid hormone receptor alpha, variant 1)
Thra_v2  (thyroid hormone receptor alpha, variant 2)
Thrb  (thyroid hormone receptor beta)


Additional Information