Differential effects of extracellular matrix on secretion of prolactin and growth hormone by rat pituitary tumour cells in vitro

1985 ◽  
Vol 108 (2) ◽  
pp. 156-160 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Growth Hormone ◽  
Extracellular Matrix ◽  
Corneal Endothelium ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Cell Protein ◽  
Thyrotrophin Releasing Hormone ◽  
Rate Of Spread ◽  
Rat Pituitary

Abstract. Two types of rat pituitary tumour cells secreting both prolactin (Prl) and growth hormone (GH) were cultured in vitro either on plastic dishes or on surfaces coated with an extracellular matrix (ECM) derived from bovine corneal endothelium. The presence of ECM caused an increase in Prl but a decrease in GH. On one cell line the Prl response to thyrotrophin releasing hormone (TRH) was increased by ECM. There was an increase in the rate of spread of the cultures, an increase in cell protein, and DNA synthesis and a change in cell morphology when ECM was used. It is suggested that these observations can be explained by a sensitizing action of ECM to growth factors present in serum.

scholarly journals Human chorionic somatomammotropin and growth hormone gene expression in rat pituitary tumour cells is dependent on proximal promoter sequences

1989 ◽  
Vol 17 (11) ◽  
pp. 4327-4337 ◽  
Author(s):  
Mark W. Nachtigal ◽  
Barbara E. Nickel ◽  
Margaret E. Klassen ◽  
Wengang Zhang ◽  
Norman L. Eberhardt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Proximal Promoter ◽  
Growth Hormone Gene ◽  
Promoter Sequences ◽  
Rat Pituitary ◽  
Chorionic Somatomammotropin

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

1980 ◽  
Vol 95 (3) ◽  
pp. 319-327 ◽  
Author(s):  
Oddvar Naess ◽  
Egil Haug ◽  
Kaare Gautvik
Keyword(s):  
Growth Hormone ◽  
Hormone Receptors ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Scatchard Analysis ◽  
Hormone Production ◽  
Single Class ◽  
High Affinity ◽  
Rat Pituitary

Abstract. The effect of corticosterone and dexamethasone on the production of growth hormone and prolactin was studied in rat pituitary tumour cells (GH3-cells) in culture. Corticosterone and dexamethasone caused a dose-dependent stimulation of growth hormone synthesis, and the highest concentration (10−6 mol/l) increased growth hormone levels to 250% of controls. This concentration, however, decreased prolactin synthesis to 25% of the control values. The cytosol fractions from monolayer cultures as well as from tumours of GH3-cells were found to possess receptor molecules for glucocorticoid hormones, having a sedimentation constant close to 8 S in a salt-free buffer and 4 S in the presence of 0.5 mol/l KCL. Isoelectric point of the receptor was 5.8. Scatchard analysis showed one single class of binding sites with high affinity (Kd 2.1 ± 0.4 (sd × 10−9 mol/l). Studies on the steroid specificity revealed that dexamethasone had the highest affinity for the receptor. Corticosterone, cortisol and progesterone had also high affinity, whereas testosterone and oestradiol-17β had no significant affinity for the receptors. After in vivo administration of [3H]dexamethasone to GH3 tumour-bearing rats, radioactivity could be extracted from purified nuclei bound to 4 S macromolecules. The presence of receptors for glucocorticosteroid hormones in the GH3-cells, suggests that these hormones may alter growth hormone and prolactin production at the anterior pituitary level.

EFFECT OF BROMOCRIPTINE, ERGOTAMINE AND OTHER ERGOT ALKALOIDS ON THE HORMONE SECRETION AND GROWTH OF A RAT PITUITARY TUMOUR

1980 ◽  
Vol 86 (1) ◽  
pp. 147-153 ◽  
Author(s):  
R. A. PRYSOR-JONES ◽  
J. S. JENKINS
Keyword(s):  
Growth Hormone ◽  
Inhibitory Action ◽  
Tumour Growth ◽  
Hormone Secretion ◽  
Ergot Alkaloids ◽  
Pituitary Tumour ◽  
Rat Pituitary ◽  
Dopaminergic Mechanisms ◽  
Excessive Secretion

The effect of bromocriptine on hormone secretion and the growth of the prolactin- and growth hormone (GH)-secreting rat pituitary tumour of the GH3 cell line has been compared with that of ergotamine and other ergot alkaloids. Bromocriptine in doses ranging from 1 to 20 mg/kg had no effect on tumour growth or on the excessive secretion of GH by the tumour; prolactin concentrations were reduced only by the highest dosage of the drug. Similarly the tumour was resistant to the administration of ergocryptine, ergocornine and the synthetic ergolines, lergotrile and CH 29–717. In contrast, ergotamine reduced secretion of both GH and prolactin and considerably inhibited the growth of the tumour. Experiments in vitro showed that ergotamine inhibited DNA synthesis of the tumour cells and decreased hormone secretion. It was concluded that ergotamine had a direct inhibitory action on the GH3 cell tumour which was not mediated through the dopaminergic mechanisms.

Specific antisense RNA inhibition of growth hormone production in differentiated rat pituitary tumour cells

1990 ◽  
Vol 171 (1) ◽  
pp. 293-300 ◽  
Author(s):  
Ruth H. Paulssen ◽  
Eyvind J. Paulssen ◽  
Peter Aleström ◽  
Jan O. Gordeladze ◽  
Kaare M. Gautvik
Keyword(s):  
Growth Hormone ◽  
Antisense Rna ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Hormone Production ◽  
Inhibition Of Growth ◽  
Rat Pituitary ◽  
Rna Inhibition

EFFECTS OF SEX STEROIDS ON GROWTH HORMONE PRODUCTION IN CULTURED RAT PITUITARY CELLS

1978 ◽  
Vol 87 (1) ◽  
pp. 40-54 ◽  
Author(s):  
E. Haug ◽  
K. M. Gautvik
Keyword(s):  
Growth Hormone ◽  
Sex Steroids ◽  
Pituitary Tumour ◽  
Maximum Effect ◽  
Pituitary Cells ◽  
Hormone Production ◽  
Thyrotrophin Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Dose Dependent

ABSTRACT Monolayer cultures of rat pituitary tumour cells (GH3) were used to study the effects of different sex steroids on growth hormone (GH) production expressed as the amount of extracellular hormone which accumulated during 24 h. The hormone was measured with a sensitive and specific radioimmunoassay. Oestradiol-17β (10−12 mol/l—10−6 mol/l) caused a dose-dependent decrease in GH production with the maximum effect (30 % of controls) at 10−10 mol/l. After the cessation of treatment with oestradiol-17β (10−8 mol/l for 7 days), control levels of GH were obtained within 11 days, after a transient augmentation of production. Progesterone (10−11–10−6 mol/l) caused a dose-dependent stimulation of GH production, and the maximum effect (160 % of controls) was observed at 10−6 mol/l. Testosterone (10−6 mol/l) decreased the production of GH to 70 % of control values, whereas 5α-dihydrotestosterone (DHT) had no effect. Cell growth was not affected by any of the sex steroids. Corticosterone (10−6 mol/l) increased GH production to about 400 % of control values, and this effect was inhibited by oestradiol-17β (10−6 mol/l). The hypothalamic peptides, thyrotrophin releasing hormone (TRH) and somatostatin, that both depressed GH production did not significantly inhibit the stimulatory effect of corticosterone. When used in combination, the effects of oestradiol-17β (10−6 mol/l) and TRH (3 × 10−7 mol/l) were additive which was not the case for the combination oestradiol-17β (10−6 mol/l) and testosterone (10−6 mol/l). These results suggest different mechanisms of action of peptide and steroid hormones on GH production in the GH3 cells. If the properties of the GH3 cells reflect those of normal somatotrophs the sex steroids may alter GH production at the pituitary level, an influence that may be further modulated by corticoids, TRH and somatostatin.

THE PRESENCE OF BIOSYNTHETIC PRECURSORS AND HETEROGENEOUS MESSENGER RNAs FOR PROLACTIN IN CULTURED RAT PITUITARY TUMOUR CELLS

1983 ◽  
Vol 104 (2_Supplb) ◽  
pp. S66-S69
Author(s):  
P. Aleström ◽  
E.J. Paulssen ◽  
V. Gautvik ◽  
M. Kriz ◽  
E. Haug ◽  
...  
Keyword(s):  
Pituitary Tumour ◽  
Tumour Cells ◽  
Messenger Rnas ◽  
Rat Pituitary

Prolactin secretion and dopamine receptors of the MtTW15 transplantable pituitary tumour

1982 ◽  
Vol 94 (3) ◽  
pp. 347-NP ◽  
Author(s):  
M. J. Cronin ◽  
D. A. Keefer ◽  
C. A. Valdenegro ◽  
L. G. Dabney ◽  
R. M. MacLeod
Keyword(s):  
Pituitary Gland ◽  
Dopamine Receptors ◽  
Anterior Pituitary ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cells ◽  
Dopamine Antagonist ◽  
Cell Column ◽  
Prolactin Release

The MtTW15 transplantable pituitary tumour grown in rats was tested in vitro for the ability of dopamine agonists to affect prolactin secretion and for the existence of dopamine receptors. Prolactin release from enzymatically dispersed cells and non-enzymatically treated tissue fragments of both the tumour and the anterior pituitary gland was determined in a cell perifusion column apparatus. Dopamine (0·1–5 μmol/l), bromocriptine (50 nmol/l) and the dopamine antagonist haloperidol (100 nmol/l) had no effect on prolactin release from the tumour cells. In contrast, dopamine (500 nmol/l) inhibited prolactin secretion from normal anterior pituitary cells in a parallel cell column and haloperidol blocked this inhibition. Although oestrogen treatment in vivo stimulated prolactin release in vitro when the tumour was removed and studied in the cell column, oestrogen had no effect on the inability of dopamine to modify the prolactin secretion. Growth hormone release from the tumour cells was not affected by dopamine. Although MtTW15 cells were refractory to dopaminergic inhibition of prolactin release, the dopamine receptors present in tumour homogenates were indistinguishable from the dopamine receptors previously defined in the normal anterior pituitary gland. The binding of the dopamine antagonist [3H]spiperone to the tumour was saturable (110 fmol/mg protein), of high affinity to one apparent class of sites (dissociation constant = 0·12 nmol/l), reversible and sensitive to guanine nucleotides. The pharmacology of the binding was defined in competition studies with a large number of agonists and antagonists. From the order of potency of these agents, a dopaminergic interaction was apparent. We conclude that the prolactin-secreting MtTW15 tumour cells appear to be completely unresponsive to dopamine or to the potent dopamine agonist bromocriptine, in spite of apparently normal dopamine receptors in the tumour.

Progestin receptors in prolactin and growth hormone producing tumours in rats

1982 ◽  
Vol 100 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Oddvar Naess ◽  
Egil Haug ◽  
Arne Attramadal ◽  
Kaare M. Gautvik
Keyword(s):  
Growth Hormone ◽  
Glucocorticoid Receptors ◽  
Progesterone Receptors ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Female Rats ◽  
Progestin Receptors ◽  
High Affinity ◽  
Protein Nature ◽  
Specific Receptors

Abstract. Progesterone and corticosterone have a similar effect on the production of growth hormone (GH) and prolactin (Prl) by pituitary tumour cells (GH3 cells) in culture. Previously we have shown that progesterone has a high affinity for the glucocorticoid receptors in these cells. Progesterone may therefore exert its effects through binding to the glucocorticoid receptor. The aim of the present study was to investigate if the GH3 tumour cells and an oestrogen induced pituitary tumour, which also produce GH and Prl, possess specific receptors for progesterone. Both the GH3 tumours and the oestrogen induced pituitary tumour were in fact found to possess cytoplasmatic receptor molecules for progesterone by using the potent progestin R5020 as a marker. Isoelectric focusing revealed one binding component (pH 5.9), which was of protein nature. The binding was of high affinity (Kd 2 × 10−9 mol/l). In the oestrogen induced tumour, the maximal binding was 70 fmol/mg cytosol protein. In female rats with GH3 tumours the binding was 55 fmol/mg cytosol protein. Priming of the animals with 1 mg oestradiol-valerate increased the binding to 116 fmol/mg cytosol protein, whereas very little binding was found in GH3 tumours from rats castrated 7 days before sacrifice. The receptors in the oestrogen induced pituitary tumour and the GH3 tumours exhibited high affinity for R5020 and progesterone, whereas corticosterone had no significant affinity for the receptors. Using exchange assay, it was demonstrated that the cytoplasmic progestin receptors could be translocated to the nucleus after administration of progesterone to the animals. Thus, the presence of specific progesterone receptors, different from the glucocorticoid receptors, strongly indicates that the effects of progesterone on GH and Prl production are mediated through the progesterone receptors.

Vitamin D-induction of secretory responses in rat pituitary tumour (GH4C1) cells

1988 ◽  
Vol 117 (2) ◽  
pp. 293-298 ◽  
Author(s):  
J. D. Wark ◽  
V. Gurtler
Keyword(s):  
Vitamin D ◽  
Time Course ◽  
Cell Model ◽  
Hormone Secretion ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cells ◽  
Bay K 8644 ◽  
Similar Time ◽  
Rat Pituitary

ABSTRACT 1,25-Dihydroxyvitamin D3(1,25-(OH)2D3) selectively enhances prolactin gene expression in GH4C1 clonal rat pituitary tumour cells. Because this effect requires extracellular Ca2+, we studied the effect of 1,25-(OH)2D3 on another Ca2+-dependent process, agonist-induced hormone secretion. Pretreatment with 1,25-(OH)2D3 (1 nmol/l) caused at least 25-fold sensitization of GH4C1 cells to the voltage-sensitive Ca2+ channel agonist BAY K 8644 (methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5-carboxylate) as a prolactin secretagogue. This inductive effect of 1,25-(OH)2D3 followed a similar time-course to the enhancement of prolactin production. 1,25-(OH)2D3 had no effect on basal or BAY K 8644-induced 45Ca2+ uptake. The Ca2+-selective divalent cation ionophore 11,19,21-trihydroxy-4,6,8,12,14,18,20-heptamethyl-9-oxo-22-(tetrahydro-5 methyl-5-tetra hydro-5-(1-hydroxyethyl)-5-methyl-2-furanyl)-10,16-docosadienoic acid (ionomycin; 12 nmol/l–1·2 μmol/l) caused no significant increase in prolactin secretion in the absence of 1,25-(OH)2D3, but in cells treated with 1,25-(OH)2D3-(1 nmol/l), it increased prolactin secretion by 73% at 12 nmol/l and by a maximum of 98% at 0·12 μmol/l. These data demonstrate that vitamin D markedly enhances the responsiveness of GH4C1 functional pituitary tumour cells to two secretagogues which acts primarily through Ca2+-dependent mechanisms. They support the proposal that 1,25-(OH)2D3 acts in this cultured cell model either by effecting a redistribution of intracellular Ca2+ or by increasing the response of a Ca2+ -sensitive effector system, but not by enhancing agonist-induced Ca2+ uptake. J. Endocr. (1988) 117, 293–298

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