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The present study has investigated the relative levels and interconversion of latent and active forms of transforming growth factor-β1 (TGF-β1) in human thyroid follicular cell cultures derived from sporadic non-toxic goitres. Northern blotting of RNA extracted from 72-h cultures revealed a 2·5 kb mRNA transcript hybridizing with a cDNA probe for latent TGF-β1, the intensity of which was doubled in cells exposed to Nal (10 µmol/l). Radioreceptor assay of follicular cell-conditioned medium for TGF-β1 content confirmed a similar enhancing effect of iodide. The endogenous active component of TGF-β1 present in conditioned medium represented only a minor fraction of the total TGF-β1 content, this fraction was not enhanced by exposure of follicular cells to iodide. The low level of endogenous active TGF-β1 in medium conditioned by either control or iodide-treated cells was confirmed by immunoadsorption with a precipitating antiserum against active TGF-β1, when such cells failed to show a reversal of the iodide-induced decrease in [methyl-³H]thymidine incorporation into trichloroacetic acid-precipitable material. In contrast to the inhibitory effect of iodide on de novo DNA synthesis, which appeared not to reflect an increase in active TGF-β1, the inhibitory effects of plasminogen (100 mg/l) or plasmin (2000 U/l) on [methyl-³H]thymidine incorporation into thyroid cells were reversible by TGF-β1 immunoadsorption. This provides evidence that the plasmin-mediated inhibition of DNA synthesis in thyroid follicular cells may be attributed to the growth-regulating action of an increased level of activated TGF-β1. The findings of this study therefore provide evidence that (i) human thyroid follicular cells are potentially capable of activating locally derived latent TGF-β1, (ii) an increase in thyroidal TGF-β1 mRNA and latent TGF-β1 peptide availability, following exposure of cells to iodide, is not accompanied by a corresponding increase in active TGF-β1, and (iii) within the thyroid gland, as in other epithelial tissues, activation of endogenous TGF-β1 may be dependent upon the proteolytic actions of plasmin.

Journal of Endocrinology (1994) 141, 183–190

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