Effects of pretreatment with tetradecanoyl phorbol acetate on regulation of growth hormone and prolactin secretion from ovine anterior pituitary cells

Abstract

Tetradecanoyl phorbol acetate (TPA) stimulates growth hormone (GH) and prolactin secretion from ovine anterior pituitary cells. Pretreatment of the cells with TPA abolishes this effect, presumably due to down-regulation of protein kinase C. Such pretreatment did not alter effects of thyrotropin-releasing hormone or dopamine on prolaction secretion, suggesting no involvement of protein kinase C. Pretreatment with TPA attenuated actions of GH-releasing hormone on GH release (but not actions on cyclic AMP levels), possibly due to depletion of cellular stores of GH. Such pretreatment also attenuated inhibition of GH release by somatostatin, possibly due to phosphorylation of receptors or associated proteins by protein kinase C.

Inhibition of BK channels contributes to the second phase of the response to TRH in clonal rat anterior pituitary cells

“…2002). Still, activation of PKC is not essential for induced secretion (Boyd & Wallis 1989, French et al. 1989).…”

An inward‐rectifying K+ current in clonal rat pituitary cells and its modulation by thyrotrophin‐releasing hormone.

“…Tumour-promoting phorbol esters have been shown to enhance action potential frequency in GH4C1 cells (0stberg, Sand, Bj0ro & Haug, 1986) and GH3 cells (Dufy et al 1987;Gammon, Oxford, Allen, McCarthy & Morell, 1989). Recent publications, though, give hints that TRH and phorbol ester might work in a different way to induce secretion (Gordeladze, Bj0ro, 0stberg, Sand, Torjesen, Haug & Gautvik, 1988;Gordeladze, Bj0ro, Torjesen, 0stberg, Haug & Gautvik, 1989) and that protein kinase C is not essential for hormone-induced secretion (French, Moor, Lussier & Kraicer, 1989;Boyd & Wallis, 1989). Villarroel, Marrion, Lopez & Adams (1989) found that protein kinase C is not involved in the normal bradykinin signal transduction, although activation of protein kinase C mimics bradykinin-induced inhibition of the M current in phaeochromocytoma cells.…”