HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Keijzer, R. Articles by Lamers, W. H Search for Related Content PubMed PubMed Citation Articles by Keijzer, R. Articles by Lamers, W. H

¹ Department of Pediatric Surgery, Erasmus MC-Sophia, Dr Molewaterplein 60, 3015 GJ Rotterdam, The Netherlands
² Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, Meibergdreef 69–71, 1105 AZ Amsterdam, The Netherlands
³ Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

(Requests for offprints should be addressed to W H Lamers who is now at AMC Liver Center, Academic Medical Center, University of Amsterdam, Meibergdreef 69–71, 1105 BK, Amsterdam, The Netherlands; Email: w.h.lamers{at}amc.uva.nl)

(R Keijzer and P-J E Blommaart contributed equally to this study)

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