| Research Abstract |
1. Follicles were isolated from thyroid tissues obtained at the time of operations in patients with Graves' disease. They could be cultured for months in monolayer or in suspension using a spinner flask. During the period of culture, the cells kept differentiated characters as thyrocytes, such as specific binding of TSH and TSH-dependent increase in cyclic AMP. They could be splitted and passed by trypsinization, but they lost their ability to proliferate after two or three generation period.
2. In cultured human thyrocytes, DNA synthesis was enhanced by TSH, IGF-I, and EGF dose-dependently. IGF-I significantly increased the number of TSH receptor in these cells.
3. in rat thyroid cell line FRTL-5, DNA synthesis was enhanced by TSH, IGF-I, IGF-II,TGF- , IL-I, and FGF dose-depedently. Among these stimulating activities, synergism was observed between the action of TSH and IGF-I or II. The action of TSH was inhibited by TGF- , and vice versa. IGF-I increased the number of TSH receptor dose
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-dependently. TGF- in low concentrations increased and that in high concentrations decreased it. EGF and IL-1 did not change the receptor number.
4. -subunit of 7s NGF ( NGF) inhibited the growth stimulating action of IGF-I in FRTL-5 cells. It is suggested that NGF directly acts against IGF-I molecule and decreases its ability to bind to type I IGF recptor. In conditioned media of human thyoroid cells, an inhibitory activity against IGF-I similar to NGF was observed.
5. Growth stimulating activity was detected in conditioned media of human thyroid cells. This activity, TDGF, stimulated DNA synthesis in FRTL-5 cells, human thyrocytes,and rat fibroblasts. TDGF, determined as a stimulator of DNA synthesis in FRTL-5 cells, was partly purified by gel filtration and cathion exchange. Its molecular weight was approximately 4000 and pI was 4.5, TDGF specifically bound to FRTL-5 cells. Since the binding was not inhibited by known growth factors, TDGF is likely to be an unknown, novel growth factor. Less
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