Stimulatory effects of induced phagocytosis on the function of isolated thyroid cells

Stimulation of endocytosis is a very early effect of thyrotropin on thyroid. However, the relationship of the endocytotic process to the many other thyrotropin effects on thyroid is not clearly defined. Since phagocytosis in isolated thyroid cells is a presumed model for in vivo endocytosis of colloid, we induced phagocytosis in isolated thyroid cells by incubating them at 37 degrees C with 0.109-mu diameter polystyrene microbeads; phagocytosis was confirmed in each experiment by electron microscopy and/or spectrophotometric analysis of dioxane cell extracts. Cells incubated with 50-100-mu diameter polystyrene macrobeads (too large to ingest) served as controls. Microbead-induced phagocytosis in isolated thyroid cells was consistently accompanied by increases in: (a) cyclic 3',5'-adenosine monophosphate-(14)C formation from adenine-8-(14)C (66%); (b) iodide-(131)I trapping (40%); (c) protein and RNA synthesis (30%); (d) phospholipogenesis (50%); (e) alpha-aminoisobutyric acid-1-(14)C uptake (15%). 50- to 100-mu diameter polystyrene macrobeads did not influence cell function in any of these experiments. Aminotriazole, 5 x 10(-3) (M), a peroxidase inhibitor, blocked the stimulatory effect of microbead-induced phagocytosis on phospholipogenesis only. These studies indicate that in isolated thyroid cells the phagocytotic process, per se, may alter activity of the membrane-bound adenyl cyclase enzyme. The resultant increase in cyclic 3',5'-adenosine monophosphate may be a triggering mechanism for (some) subsequent metabolic changes occuring during phagocytosis. Since these changes mimic those induced by thyrotropin, it is suggested that a variety of thyrotropin effects on thyroid may be secondary to stimulation of colloid resorption and hormone secretion.