Effects of cortisol, 17β‐estradiol and thyroliberin on prolactin and growth hormone production, cell grwoth and cell cycle distribution in cultured rat pituitary tumour cells

Abstract

Prolactin and growth hormone production were measured in a rat pituitary tumour cell strain (GH,) after treatment with cortisol (5 X MI, thyroliberin (2.5 x M) and l7P-estradiol M). The changes in hormone production were related to alterations in cell growth rate and cell cycle distribution. Cortisol inhibited prolactin production, stimulated growth hormone production and reduced the cellular growth rate measured two days after start of treatment (maximum about 40% inhibition). Flow-micro fluorometric analysis of DNA distributions showed that cortisol treatment reduced the relative number of cells in S phase (maximum effect about 50%) with a compensatory increase of the proportion of cells in Gl phase. The lack of inhibition of prolactin production after three days of cortisol treatment may partly be related to the increased number of cells in G, phase. Thyroliberin and 17P-estradiol did not significantly affect cell growth after six days of treatment, although the fraction of cells in S phase was reduced by approximately 40% with a corresponding increase of cells in Gl phase. For thyroliberin and 17P-estradiol, the stimulatory effect on prolactin production and the inhibitory effect on growth hormone production within a period of treatment of six days cannot be explained by a shift in cell cycle distributions. None of the three hormones influenced the growth fraction which was equal to unity.In conclusion, thyroliberin and 17P-estradiol are able to change prolactin and growth hormone production without altering the cell cycle distribution. However, the effects of cortisol on prolactin and growth hormone production may partly be due to an alteration in cell cycle traverse resulting in an increased number of cells in the G1 phase.

Effects of thyroliberin (TRH) on cell proliferation and prolactin secretion by GH3/B6 rat pituitary cells: A comparison between serum‐free and serum‐supplemented media

“…As previously shown (Tashjian et al, 1971;Clausen et al;1971) the total amount of proteinldish was unaffected by TRH (13 nM) at least during the first 4 days. However, the protein content per $ 2 0 a:g& ?…”

Glucocorticoid receptors and cell cycle progression in human melanoma cell lines

“…G1 arrest by glucocorticoid is a well known effect in lymphoid cells (Harmon et al, 1979) and has also been reported in rat pituitary tumor cells (Clausen et al, 1978), SV40-3T3 cells (Young and Dean, 1980), HeLa cells (Kollmorgen and Griffin, 19691, and NHIK 3025 cervix carcinoma cells (Bakke and Eik-Nes, 1981). The instantaneously abolished increase in the percentage (3H)thymidine-labeled M-5A cells after dexamethasone (Fig.…”

Effects of glucocorticosteroids on prolactin and growth hormone production and characterization of the intracellular hormone receptors in rat pituitary tumour cells

“…Furthermore, our results confirm the previous observation that glucocorticoid hor¬ mones stimulate GH synthesis in GH3-cells (Ban¬ croft et al 1969), as well as GH synthesis in long-term cultures on monkey pituitary glands (Kohler et al 1968 (Munck 1971;Loeb 1976). In the GHs-cells we (Clausen et al 1978) have previously demonstrated that cor¬ tisol treatment inhibited cell proliferation by reduc¬ ing the relative number of cells in the S phase of growth, leading to a transient accumulation of cells in the Gi phase without changing the total proliferative pool of cells. Since the fraction of hormoneproducing cells in the Gi phase is probably larger than in the S phase, the cortisol stimulated increase in GH production may partly be related to a shift in the phase of cell growth.…”