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

✍ Scribed by O. P. F. Clausen; K. M. Gautvik; E. Haug

• Publisher: John Wiley and Sons
• Year: 1978
• Tongue: English
• Weight: 818 KB
• Volume: 94
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1040940210

✦ Synopsis

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.