Effects of antimicrotubule agents, potassium and inhibitors of energy production on hCG secretion.
The BeWo trophoblastic cell line was employed to assess the requirement for microtubules and cellular energy in human chorionic gonadotropin (hCG) secretion. In contrast to the general inhibitory effect of colchicine and vincristine on hormone secretion in systems involving exocytosis, wide concentration ranges of these antimicrotubule agents caused enhancement of hCG secretion. Similarly, cytochalasin B, an agent that interferes with microfilament function, doubled both basal hCG secretion, and secretion of hCG stimulated by 1 mM dibutyryl cyclic AMP plus 1 mM theophylline (dbT). Inhibitors of cellular energy production (2,4-dinitrophenol, malonate, azide) decreased both secreted and cellular levels of hormone. High concentrations of K+ gave no enhancement of basal or dbT-stimulated hCG secretion, nor any reduction of cellular hCG levels. These findings contrasted with observations of others in secretory systems involving exocytosis, in which high K+ potentiated basal or stimulated hormone release and depleted cellular stores of hormone. It was concluded that the process of hCG secretion in the malignant trophoblast is fundamentally different from the mechanism of protein hormone secretion in other tissues.
D001386:Azides / Q000494:pharmacology; D002460:Cell Line; D006063:Chorionic Gonadotropin / Q000378:metabolism*; D003078:Colchicine / Q000494:pharmacology*; D003571:Cytochalasin B / Q000494:pharmacology*; D003599:Cytoskeleton / Q000502:physiology; D004140:Dinitrophenols / Q000494:pharmacology; D004734:Energy Metabolism; D008314:Malonates / Q000494:pharmacology; D008870:Microtubules / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D014750:Vincristine / Q000494:pharmacology
D001386:Azides; D006063:Chorionic Gonadotropin; D004140:Dinitrophenols; D008314:Malonates; D003571:Cytochalasin B; D014750:Vincristine; D011188:Potassium; D003078:Colchicine