Bombesin stimulates prolactin secretion from cultured rat pituitary tumour cells (GH4C1) via activation of phospholipase C

1987 ◽  
Vol 19 (3-4) ◽  
pp. 169-182 ◽  
Author(s):  
T. Bjøro ◽  
P.A. Torjesen ◽  
B.C. Østberg ◽  
O. Sand ◽  
J-G. Iversen ◽  
...  
Keyword(s):  
Phospholipase C ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cells ◽  
Rat Pituitary

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

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.

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.

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