In the rat, chronic TSH stimulation leads to self-limited thyroid
hyperplasia, goitrogenesis, and TSH-responsive thyroid
tumors. The current studies were aimed at clarifying the mechanism by which
hormone-responsive, proliferating follicular cells arise in quiescent plateau phase rat
goiters. Enzymatically monodispersed rat thyrocytes from early plateau phase and involuting
goiters were analyzed for the capacity to form thyroid follicular units after
transplantation into syngeneic recipients.
Goiters induced with two different regimens contained substantial numbers of cells capable of proliferating into functioning thyroid follicular tissue after
transplantation. The clonogenic fractions of cells from
goiters induced by
3-amino-1,2,4-triazole or KClO4/Remington low
iodine diet were significantly lower than that of cells from control glands. Furthermore, the clonogenic fraction of cells from the KClO4
goiters was also found to be significantly less than that of cells from
aminotriazole goiters despite similar TSH levels in the cell donors. The
hormone responsiveness of the clonogenic
goiter cells and the histological appearance and functional capacity of the thyroid tissue which arose after grafting were indistinguishable from controls. We conclude that the capacity to clonally proliferate into follicular units is a specific trait which characterizes a unique subset of follicular cells and speculate that the
hormone-responsive
tumors which typically appear in the chronically stimulated rat thyroid originate from cells within this subset.