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Am J Physiol Endocrinol Metab (May 13, 2003). doi:10.1152/ajpendo.00519.2002
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Submitted on November 22, 2002
Accepted on May 1, 2003

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

Helen C Cocks1, Stuart Thompson1, Frances E Turner1, Ann Logan1, Jayne A Franklyn1, John C Watkinson1, and Margaret C Eggo1*

1 Division of Medical Science, University of Birmingham, Birmingham, United Kingdom

* To whom correspondence should be addressed. E-mail: M.C.Eggo{at}bham.ac.uk.

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 measured by cell counting, and inhibited thyroid function, 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 4h and protein expression by 8h. 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 2h. This effect was enhanced when cells were cultured in TSH (4.4 fold). We conclude that TSH stimulates FGFR1 but not FGF-2 expression. PKC activation stimulates FGF-2 synthesis and secretion and TSH synergises with PKC activators. Increases in FGFR1 or FGF-2 and both may contribute to goitrogenesis.




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