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Am J Physiol Endocrinol Metab 285: E460-E469, 2003. First published May 13, 2003; doi:10.1152/ajpendo.00519.2002
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Role and regulation of the fibroblast growth factor axis in human thyroid follicular cells

Helen C. Cocks, Stuart Thompson, Frances E. Turner, Ann Logan, Jayne A. Franklyn, John C. Watkinson, and Margaret C. Eggo

Division of Medical Science, University of Birmingham, Birmingham B15 2TT, United Kingdom

Submitted 22 November 2002 ; accepted in final form 1 May 2003

Thyroidal levels of fibroblast growth factor-2 (FGF-2) and fibroblast growth factor receptor 1 (FGFR1) are elevated in human thyroid hyperplasia. To understand the significance of this, effects of FGFR1 activation on normal human thyrocyte growth and function in vitro and the regulation of FGF-2 and FGFR1 expression have been examined. FGF-2 stimulated cell growth, as measured by cell counting, and inhibited thyroid function as measured by 125I uptake. Sensitivity to FGF-2 disappeared after 7 days, although FGFR1 expression was maintained. Thyroid-stimulating hormone (TSH, 300 mU/l) increased FGFR1 mRNA expression within 4 h and protein expression by 8 h. Exogenous FGF-2 decreased FGFR1 protein. Endogenous FGF-2 levels were low (~1-2 pg/µg protein), and TSH treatment decreased these by 50%. Protein kinase C (PKC) activation increased FGF-2 mRNA and FGF-2 secretion within 2 h. This effect was enhanced (4.4-fold) when cells were cultured in TSH. We conclude that TSH stimulates FGFR1 but not FGF-2 expression. PKC activation stimulates FGF-2 synthesis and secretion, and TSH synergizes with PKC activators. Increases in FGFR1 or FGF-2 or in both may contribute to goitrogenesis.

thyrocyte; fibroblast growth factor-2; fibroblast growth factor receptor 1; protein kinase C; thyroid function; humans


Address for reprint requests and other correspondence: M. C. Eggo, The Medical School, Univ. of Birmingham, Birmingham B15 2TT, UK (E-mail: M.C.Eggo{at}bham.ac.uk).




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