title: Transforming growth factor beta regulates thyroid growth. Role in the pathogenesis of nontoxic goiter.
abstract: The production and growth regulatory activity of transforming growth factor beta were studied in human thyroid tissue. As estimated by its mRNA expression in fresh tissue samples, transforming growth factor beta was produced in normal and in diseased thyroid glands. Transforming growth factor beta mRNA was mainly produced by thyroid follicular cells and in lesser quantities by thyroid infiltrating mononuclear cells. The concentrations of transforming growth factor beta mRNA were lower in iodine-deficient nontoxic goiter than in Graves' disease and normal thyroid tissue. Transforming growth factor beta protein secretion by cultured thyroid follicular cells was also low in nontoxic goiter, but could be increased by addition of sodium iodide (10 microM) to the culture medium. Recombinant transforming growth factor beta did not affect basal tritiated thymidine incorporation in cultured thyroid follicular cells, but inhibited, at a concentration of 10 ng/ml, the growth stimulatory influence of insulin-like growth factor I, epidermal growth factor, transforming growth factor alpha, TSH, and partly that of normal human serum on cultured thyroid follicular cells. This inhibition was greater in Graves' disease than in nontoxic goiter. These results suggest that transforming growth factor beta may act as an autocrine growth inhibitor on thyroid follicular cells. Decreased transforming growth factor beta production and decreased responsiveness to transforming growth factor beta may be cofactors in the pathogenesis of iodine-deficient nontoxic goiter.
authors.affiliation: Charing Cross Sunley Research Centre, London, United Kingdom.
authors.forename: B
authors.initials: B
authors.lastname: Grubeck-Loebenstein
authors.forename: G
authors.initials: G
authors.lastname: Buchan
authors.forename: R
authors.initials: R
authors.lastname: Sadeghi
authors.forename: M
authors.initials: M
authors.lastname: Kissonerghis
authors.forename: M
authors.initials: M
authors.lastname: Londei
authors.forename: M
authors.initials: M
authors.lastname: Turner
authors.forename: K
authors.initials: K
authors.lastname: Pirich
authors.forename: R
authors.initials: R
authors.lastname: Roka
authors.forename: B
authors.initials: B
authors.lastname: Niederle
authors.forename: H
authors.initials: H
authors.lastname: Kassal
mesh_terms: D000328:Adult; D002455:Cell Division; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D015342:DNA Probes; D005260:Female; D006042:Goiter / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006111:Graves Disease / Q000503:physiopathology; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D007455:Iodine / Q000172:deficiency; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization; D012333:RNA, Messenger / Q000096:biosynthesis; D012974:Sodium Iodide / Q000494:pharmacology; D013961:Thyroid Gland / Q000473:pathology* / Q000503:physiopathology; D013972:Thyrotropin / Q000494:pharmacology; D014158:Transcription, Genetic; D015291:Transforming Growth Factors / Q000235:genetics / Q000494:pharmacology / Q000502:physiology*
chemical_list: D015342:DNA Probes; D006133:Growth Substances; D012333:RNA, Messenger; D015291:Transforming Growth Factors; D013972:Thyrotropin; D004247:DNA; D007455:Iodine; D012974:Sodium Iodide