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) All Versions of this Article: 73/3/396    most recent biolreprod.105.041426v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Holsberger, D. R. Articles by Cooke, P. S. Search for Related Content PubMed PubMed Citation Articles by Holsberger, D. R. Articles by Cooke, P. S. Agricola Articles by Holsberger, D. R. Articles by Cooke, P. S.

Regulation of Neonatal Sertoli Cell Development by Thyroid Hormone Receptor 1¹

Department of Veterinary Biosciences³ Division of Nutritional Sciences,⁴ University of Illinois,Urbana, Illinois 61802

Neonatal hypothyroidism increases adult Sertoli cell populations by extending Sertoli cell proliferation. Conversely, hyperthyroidism induces premature cessation of Sertoli cell proliferation and stimulates maturational events like seminiferous tubule canalization. Thyroid hormone receptors 1 and ß1, which are commonly referred to as TR1 and TRß1, respectively, are expressed in neonatal Sertoli cells. We determined the relative roles of TR1 and TRß1 in the thyroid hormone effect on testicular development and Sertoli cell proliferation using Thra knockout (TRKO), Thrb knockout (TRßKO), and wild-type (WT) mice. Triiodothyronine (T₃) treatment from birth until Postnatal Day 10 reduced Sertoli cell proliferation to minimal levels in WT and TRßKO mice versus that in their untreated controls, whereas T₃ had a diminished effect on TRKO Sertoli cell proliferation. Seminiferous tubule patency and luminal diameter were increased in T₃-treated WT and TRßKO testes. In contrast, T₃ had no effect on these parameters in TRKO mice. In untreated adult TRKO mice, Sertoli cell number, testis weight, and daily sperm production were increased or trended toward an increase, but the increase in magnitude was smaller than that seen in WT mice following neonatal hypothyroidism. Conversely, in TRßKO mice, Sertoli cell number, testis weight, and daily sperm production were similar to those in untreated WT mice. In addition, Sertoli cell number and testis weight in adult WT and TRßKO mice showed comparable increases following hypothyroidism. Our results show that TRKO mice have testicular effects similar to those seen in WT mice following neonatal hypothyroidism and that TRßKO mice, but not TRKO mice, have normal Sertoli cell responsiveness to T₃. Thus, effects of exogenous manipulation of T₃ on neonatal Sertoli cell development are predominately mediated through TR1.

Sertoli cells, testis

² Correspondence: Paul S. Cooke, Department of Veterinary Biosciences, 2001 S. Lincoln Ave., University of Illinois at Urbana-Champaign, Urbana, IL 61802. FAX: 217 244 1652; p-cooke{at}uiuc.edu

This article has been cited by other articles:

				A. Zamoner, K. P. Barreto, D. W. Filho, F. Sell, V. M. Woehl, F. C. R. Guma, R. Pessoa-Pureur, and F. R. M. B. Silva Propylthiouracil-induced congenital hypothyroidism upregulates vimentin phosphorylation and depletes antioxidant defenses in immature rat testis J. Mol. Endocrinol., March 1, 2008; 40(3): 125 - 135. [Abstract] [Full Text] [PDF]