Role and regulation of the fibroblast growth factor axis in human thyroid follicular cells

Helen Cocks, Stuart Thompson, FE Turner, James Ramsden, Ann Logan, Jayne Franklyn, John Watkinson, Margaret Eggo

Research output: Contribution to journalArticle

13 Citations (Scopus)


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 (approximately 1-2 pg/microg 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.
Original languageEnglish
Pages (from-to)E460-E469
JournalAmerican Journal of Physiology: Endocrinology and Metabolism
Publication statusPublished - 1 Jan 2003


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


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