Radioimmunoassay detection of endorphins from long-term culture of human pituitary tumour cells

1982 ◽  
Vol 99 (2) ◽  
pp. 174-178 ◽  
Author(s):  
Burt Sharp ◽  
Shlomo Melmed ◽  
Ronald Goldberg ◽  
Harold E. Carlson ◽  
Samuel Refetoff ◽  
...  
Keyword(s):  
Human Serum ◽  
Opioid Peptides ◽  
Anterior Pituitary ◽  
Monolayer Culture ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Human Pituitary ◽  
Long Term Culture ◽  
Normal Human

Abstract. Using a sensitive and precise radioimmunoassay for human β-endorphin, we have demonstrated the sustained secretion of opioid peptides from human pituitary tumour cells. Pituitary tumour tissue obtained from a patient with Nelson's syndrome was maintained in continuous monolayer culture and secreted both β-lipotropin and β-endorphin, with predominance of the latter. This is compatible with the idea that the β-endorphin in normal human serum is secreted as such despite the predominance of β-lipotropin compared with β-endorphin in the anterior pituitary.

INHIBITION BY HUMAN SERUM OF THE ADIPOKINETIC EFFECT OF A HUMAN PITUITARY LIPID-MOBILIZING FACTOR

1972 ◽  
Vol 71 (3) ◽  
pp. 443-453 ◽  
Author(s):  
Olav Trygstad ◽  
Irene Foss
Keyword(s):  
Human Serum ◽  
Gel Filtration ◽  
Deae Cellulose ◽  
Inhibitory Effect ◽  
Disc Electrophoresis ◽  
Inhibitory Protein ◽  
Human Pituitary ◽  
Albumin Fraction ◽  
Pituitary Glands ◽  
Normal Human

ABSTRACT A lipid-mobilizing factor (LMF) with an adipotrophic effect in human and animal fat tissue has been prepared from human pituitary glands. The addition of normal human serum to LMF reduced its lipolytic effect, and it was completely abolished by serum from a group of obese patients, whereas the lipolysis was not influenced by serum from patients with generalized lipodystrophy. By DEAE-cellulose chromatography of human serum the inhibitory effect on LMF was found to be present in a protein fraction less acidic than the main serum albumin fraction. The inhibitory fraction was deprived of some contaminants by Sephadex gel filtration. Disc electrophoresis demonstrated the presence of three components in the inhibitory protein (IP), and they were identified as albumin, transferin, and haemopexin by immuno-electrophoresis. Precipitation of these proteins by their rabbit antisera demonstrated that the inhibitory effect was present in the albumin fraction. Insulin like activity was not observed in IP. A protein binding of LMF by IP could not be demonstrated. Incubation at 37°C for one hour of a mixture of LMF and IP eliminated the electrophoretic picture of LMF. It is concluded that the inhibitory effect of human serum may be due to proteolysis of LMF.

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.

Carcinoid tumour cells in long-term culture: Release of serotonin but not of tachykinins on stimulation with adrenoceptor agonists

1988 ◽  
Vol 42 (4) ◽  
pp. 506-510 ◽  
Author(s):  
H. Ahlman ◽  
L. Åhlund ◽  
O. Nilsson ◽  
G. Skolnik ◽  
E. Theodorsson ◽  
...  
Keyword(s):  
Carcinoid Tumour ◽  
Tumour Cells ◽  
Long Term Culture ◽  
Adrenoceptor Agonists

BROMOCRIPTINE SUPPRESSES ACTH SECRETION FROM HUMAN PITUITARY TUMOUR CELLS IN CULTURE BY A DOPAMINERGIC MECHANISM

1981 ◽  
Vol 15 (5) ◽  
pp. 479-484 ◽  
Author(s):  
E. F. ADAMS ◽  
M. J. ASHBY ◽  
SUSAN M. BROWN ◽  
M. C. WHITE ◽  
K. MASHITER
Keyword(s):  
Pituitary Tumour ◽  
Tumour Cells ◽  
Acth Secretion ◽  
Human Pituitary ◽  
Cells In Culture ◽  
Dopaminergic Mechanism

Binding of ovine 125I-prolactin to cultured anterior pituitary tumour cells and normal cells

Nature ◽  
1975 ◽  
Vol 255 (5510) ◽  
pp. 636-638 ◽  
Author(s):  
WILLIAM L. FRANTZ ◽  
P. PAYNE ◽  
O. DOMBROSKE ◽  
CARLOS SONNENSCHEIN
Keyword(s):  
Anterior Pituitary ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Normal Cells

Long-term culture of normal human kidney glomerular cells

1992 ◽  
Vol 28 (7-8) ◽  
pp. 471-474 ◽  
Author(s):  
Ruth E. Gibson-D’Ambrosio ◽  
Steven M. D’Ambrosio
Keyword(s):  
Human Kidney ◽  
Long Term Culture ◽  
Normal Human Kidney ◽  
Normal Human

Studies on the glucocorticoid-receptor blocking action of RU 38486 in cultured ACTH-secreting human pituitary tumour cells and normal rat pituitary cells

1985 ◽  
Vol 109 (1) ◽  
pp. 64-69 ◽  
Author(s):  
S. W. J. Lamberts ◽  
E. G. Bons ◽  
P. Uitterlinden
Keyword(s):  
Pituitary Tumour ◽  
Tumour Cells ◽  
Pituitary Cells ◽  
Human Pituitary ◽  
Inhibiting Effect ◽  
Rat Pituitary ◽  
Normal Rat ◽  
Rat Pituitary Cells ◽  
Acth Secreting ◽  
Acth Release

Abstract. The glucocorticoid-receptor blocking actions of RU 38486, a new compound with anti-progesterone activity, have been investigated in cultured human ACTH-secreting pituitary tumour cells and normal rat pituitary cells. Pre-incubation of human pituitary tumour cells for 24 h with RU 38486 (1 μm) did not influence basal or CRF-stimulated ACTH release. RU 38486 (100 nm–1 μm) significantly overcame or prevented the dexamethasone (100 nm–1 μm)-induced inhibition of CRF-stimulated ACTH release by the cultured tumour cells prepared from 2 patients with Cushing's disease. The tumour cells of a third patient were insensitive to CRF. Pre-incubation for 24 h with 1 μm RU 38486 facilitated CRF-stimulated ACTH release significantly. Studies with cultured normal rat pituitary cells showed that the inhibiting effect of 24 h pre-incubation with 10 and 50 nm dexamethasone on CRF-stimulated ACTH release could be acutely (measured over 4 h) overruled in a dose-dependent way by RU 38486 (100 nm, 1 and 10 μ), while pre-incubation for 24 h of these cells with RU 38486 (100 nm and 1 μm) significantly attenuated the acute inhibiting effect of 1 μm dexamethasone on CRF-stimulated ACTH-release. The results of these in vitro experiments are discussed against the background of the possible therapeutic use RU 38486 in patients with Cushing's syndrome in order to block the deleterious effects of high circulating cortisol concentrations.

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