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Thyroglobulin suppresses thyroid-specific gene expression in cultures of normal but not neoplastic human thyroid
Yuko Ishido1, Kazuko Yamazaki, Makoto Kammori
1Laboratory of Molecular Diagnostics (Y.I., Y.L., K.S.), Department of Mycobacteriology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo 189-0002, Japan; Thyroid Disease Institute (K.Y., M.K., Y.S., E.Y, T.Y.), Kanaji Thyroid Hospital, Tokyo 114-0015, Japan; and Department of Medicine (D.F.S.), Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
Context:
It was shown in the rat thyroid that thyroglobulin (Tg) stored in the follicular lumen is a potent regulator of thyroid-specific gene expression to maintain the function of individual follicles. However, the actions of Tg as a regulatory molecule in human thyroid have not been studied.
Objective:
Our objective was to determine the effect of Tg on gene expression in normal and diseased human thyroid and to examine whether the proposed model of negative-feedback autocrine regulation of thyroid function by Tg is applicable in the human as well as the rat.
Design:
Primary cultures of human thyrocytes were established from normal thyroid, Graves' disease thyroid, adenomatous goiter, follicular adenoma, and papillary carcinoma tissues obtained during surgery. Cells were stimulated with physiologic (ie, follicular) concentrations of Tg, and mRNA and protein expression of genes involved in thyroid hormonogenesis were evaluated. The effects of Tg on thyroid-specific gene expression were also assessed in 2 human papillary carcinoma cell lines.
Results:
Transcript levels of genes participating in thyroid hormone biosynthesis were significantly reduced by Tg in thyrocyte cultures derived from normal and Graves' thyroid, but not in cultures derived from thyroid neoplasms and adenomatous goiter.
Conclusion:
It was confirmed that Tg acts as a negative-feedback regulator of gene expression in human thyrocytes, suggesting that Tg signaling may constitute a common mechanism for maintaining thyroid homeostasis in species with follicular thyroid morphology. However, certain diseases of intrinsic thyroid overgrowth appear to be associated with an escape from the regulatory mechanism of Tg.
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