Eur J Endocrinol
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DOI: 10.1530/eje.1.02111
European Journal of Endocrinology, Vol 154, Issue 3, 491-500
Copyright © 2006 by European Society of Endocrinology
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EXPERIMENTAL STUDY

Novel neuroanatomical pathways for thyroid hormone action in the human anterior pituitary

Anneke Alkemade1,2, Edith C Friesema3, George G Kuiper3, Wilmar M Wiersinga1, Dick F Swaab2, Theo J Visser3 and Eric Fliers1,2

1 Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, 1105 AZ, The Netherlands, 2 Netherlands Institute for Brain Research, Amsterdam, 1105 AZ, The Netherlands and 3 Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands

(Corresponding should be addressed to E Fliers; Email: e.fliers{at}amc.uva.nl)

Objective: An increasing number of proteins appear to be involved in thyroid hormone feedback action at the level of the anterior pituitary, but the cell types expressing these proteins are largely unknown. The aim of the present study was to identify cell types in the human anterior pituitary that express type II and type III deiodinase (D2 and D3), the recently described thyroid hormone transporter (MCT8) and thyroid hormone receptor (TR) isoforms by means of double-labeling immunocytochemistry.

Results: We found TR isoforms to be expressed most prominently in gonadotropes and – although to a lesser extent – in thyrotropes, corticotropes, lactotropes and somatotropes. D3 staining showed a distribution pattern that was remarkably similar. By contrast, D2 immunoreactivity was observed exclusively in folliculostellate (FS) cells showing coexpression with human leukocyte antigen (HLA), a marker of major histocompatibility complex (MHC)-class II. MCT8 immunostaining was present in FS cells without HLA coexpression.

Conclusions: From these results, we propose a novel neuroanatomical model for thyroid hormone feedback on the human pituitary, with a central role for FS cells in thyroid hormone activation, which thus play an important role in the suppression of TSH secretion by circulating thyroxine (T4).




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