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Endocrinology Vol. 141, No. 1 340-345
Copyright © 2000 by The Endocrine Society

ARTICLES

Developmental Regulation of Thyrotropin Receptor Gene Expression in the Fetal and Neonatal Rat Thyroid: Relation to Thyroid Morphology and to Thyroid-Specific Gene Expression1

Rosalind S. Brown, Victoria Shalhoub2, Sarah Coulter, Sharon Alex, Isabelle Joris, William De Vito, Jane Lian and Gary S. Stein

Departments of Pediatrics (R.S.B., S.C.), Cell Biology (V.S., J.L., G.S.S.), Pathology (I.J.), and Medicine (W.D.V., S.A.), University of Massachusetts Medical School, Worcester Massachusetts 01655

Address all correspondence and requests for reprints to: Rosalind S. Brown, M.D., Department of Pediatrics, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, Massachusetts 01655. E-mail: rosalind.brown{at}banyan.ummed.edu

The TSH receptor plays a pivotal role in thyroid gland function, growth, and differentiation, but little is known about its role or regulation in the fetus and neonate. To explore these questions, we systematically evaluated TSH receptor gene expression at the level of messenger RNA (mRNA) in thyroid glands obtained from rat fetuses and neonates, from 14 days gestation to day 5 of postnatal life. Results were compared with histological evidence of differentiation and to thyroid-specific gene expression. Northern blot and RT-PCR analysis revealed that TSH mRNA was first detected at low levels on fetal day 15, but it increased 3- to 15-fold on fetal days 17–18. Up-regulation of TSH receptor mRNA on fetal day 17–18 was accompanied by the first appearance of colloid formation and of follicular development on morphological examination. It was also paralleled by increased expression of the thyroid-specific genes thyroglobulin (Tg) and thyroid peroxidase. Unexpectedly, TSH mRNA abundance was 2- to 3-fold higher in pregnant dams than in nonpregnant adult females or adult males.

In view of the 8-day lapse between the first appearance of the thyroid diverticulum and up-regulation of TSH receptor gene expression, we conclude that pituitary TSH, acting through its receptor, plays an important role in terminal thyroid maturation, but it is not involved earlier in gestation. Similarly, these data support previous evidence that the weak thyrotropic activity of human CG could not be of significance in early fetal thyroid gland development. The increased TSH receptor mRNA on fetal day 17–18 may be attributable to up-regulation by TSH, which is first secreted into the fetal circulation at this time. The significance of the increased TSH receptor expression during pregnancy remains to be explored.




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