Vasoactive intestinal peptide increases intracellular free calcium in rat and human pituitary tumour cells in vitro

1987 ◽  
Vol 114 (1) ◽  
pp. 119-123 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Cell Line ◽  
Vasoactive Intestinal Peptide ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cells ◽  
Tumour Cell Line ◽  
Free Calcium ◽  
Human Pituitary ◽  
Epithelial Growth Factor

ABSTRACT Prolactin secretion by a human pituitary tumour cell line produced in our laboratory was stimulated by TRH, vasoactive intestinal peptide (VIP) and epithelial growth factor (EGF). All raised the intracellular concentration of free calcium (Ca2+i) of cells loaded with a fluorescent quinoline Ca2+ indicator in suspension, but the effect of TRH was much more rapid and less prolonged than that of VIP and EGF. Both TRH and VIP also increased Ca2+i in GH3 rat pituitary tumour cells, but in this cell line the effect of VIP was only found in attached cells grown on cover-slips. In both human and rat cell lines, the increase in Ca2+i produced by TRH was independent of extracellular calcium, whereas this was a requirement for the action of VIP and EGF. It is concluded that the prolactin secretogogues, VIP and probably EGF, increase Ca2+i through an effect on plasma membrane calcium channels and that this effect differs from that of TRH. J. Endocr. (1987) 114, 119–123

Oestradiol, vasoactive intestinal peptide and fibroblast growth factor in the growth of human pituitary tumour cells in vitro

1989 ◽  
Vol 120 (1) ◽  
pp. 171-177 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Fibroblast Growth Factor ◽  
Vasoactive Intestinal Peptide ◽  
Fibroblast Cell ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Fibroblast Growth ◽  
Human Pituitary

ABSTRACT The growth of two human prolactin-secreting cell lines developed in our laboratory has been investigated in response to a number of factors. Oestrogen stimulated the synthesis of DNA and protein and increased prolactin secretion. Dexamethasone had the opposite effect to oestrogen. In the presence of serum, epidermal growth factor (EGF) inhibited cell growth at concentrations of 5 ng/ml. Known secretagogues of prolactin (vasoactive intestinal peptide (VIP), TRH, bombesin and neurotensin) were investigated for their action on cell growth but only VIP had a stimulatory effect. Two preparations of fibroblast growth factor (FGF) were studied. One form, derived from bovine pituitary glands, stimulated human pituitary cell growth. In contrast, another FGF, of the basic type (rFGF), was inhibitory to cell growth, increasing the time for cell doubling from 30 to 72 h. This inhibitory effect of rFGF was modified but not abolished by serum, oestradiol, platelet-derived growth factor or EGF. We conclude that bovine pituitary contains at least two fibroblast growth factors, both of which stimulate fibroblast cell growth, but one stimulates and the other inhibits human pituitary tumour cell growth. Journal of Endocrinology (1989) 120, 171–177

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.

Defective dopaminergic regulation of prolactin secretion in a rat pituitary tumour cell line

Nature ◽  
1977 ◽  
Vol 266 (5603) ◽  
pp. 640-641 ◽  
Author(s):  
W. B. MALARKEY ◽  
J. C. GROSHONG ◽  
G. E. MILO
Keyword(s):  
Cell Line ◽  
Tumour Cell ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cell Line ◽  
Rat Pituitary ◽  
Dopaminergic Regulation

ACTH, LPH and β-Endorphin Secretion from Perfused Isolated Human Pituitary Tumour Cells in vitro

1980 ◽  
Vol 13 (4-5) ◽  
pp. 280-290 ◽  
Author(s):  
Glenda Gillies ◽  
Sally Ratter ◽  
Ashley Grossman ◽  
R. Gaillard ◽  
P.J. Lowry ◽  
...  
Keyword(s):  
Pituitary Tumour ◽  
Tumour Cells ◽  
Human Pituitary ◽  
Beta Endorphin

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

scholarly journals Pre-metastatic niche triggers SDF-1/CXCR4 axis and promotes organ colonisation by hepatocellular circulating tumour cells via downregulation of Prrx1

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Yujun Tang ◽  
Yishi Lu ◽  
Yuan Chen ◽  
Lei Luo ◽  
Lei Cai ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Lentiviral Vector ◽  
Tumour Cells ◽  
Clinical Samples ◽  
Circulating Tumour Cells ◽  
Metastatic Niche ◽  
Metastatic Sites

Abstract Background Circulating tumour cells (CTCs), especially mesenchymal CTCs, are important determinants of metastasis, which leads to most recurrence and mortality in hepatocellular carcinoma (HCC). However, little is known about the underlying mechanisms of CTC colonisation in pre-metastatic niches. Methods Detection and classification of CTCs in patients were performed using the CanPatrol™ system. A lentiviral vector expressing Prrx1-targeting shRNA was constructed to generate a stable HCC cell line with low expression of Prrx1. The effect of Prrx1 knockdown on stemness, migration, and drug resistance of the cell line was assessed, including involvement of SDF-1/CXCR4 signalling. Promising clinical applications of an inhibitor of STAT3 tyrosine phosphorylation, C188–9, and specific blockade with CXCR4 antibody were explored. Results The number of mesenchymal CTCs in blood was closely associated with tumour recurrence or metastasis. Pre-metastatic niche-derived SDF-1 could downregulate Prrx1, which induced the stemness, drug resistance, and increased expression of CXCR4 in HCC cells through the STAT3 pathway in vitro. In vivo, mice bearing tumours of Prrx1 low-expressing cells had significantly shorter survival. In xenograft tumours and clinical samples, loss of Prrx1 was negatively correlated with increased expression of CXCR4 in lung metastatic sites compared with that in the primary foci. Conclusions These findings demonstrate that decreased expression of Prrx1 stimulates SDF-1/CXCR4 signalling and contributes to organ colonisation with blood CTCs in HCC. STAT3 inhibition and specific blockade of CXCR4 have clinical potential as therapeutics for eliminating organ metastasis in advanced HCC.

Interleukin-1β induces nitric oxide production by a mouse pituitary tumour cell line (AtT20/D16)

1993 ◽  
Vol 138 (3) ◽  
pp. 429-435 ◽  
Author(s):  
K. Ohta ◽  
Y. Hirata ◽  
T. Imai ◽  
F. Marumo
Keyword(s):  
Cell Line ◽  
Tumour Cell ◽  
Pituitary Tumour ◽  
No Synthase ◽  
Tumour Cell Line ◽  
Dependent Manner ◽  
Mouse Pituitary ◽  
Dose Dependent ◽  
Inducible Nos ◽  
Acth Release

ABSTRACT To elucidate whether anterior pituitary cells express the nitric oxide (NO) synthase gene, we studied the synthesis of NO and the expression of NO synthase (NOS) mRNA by a mouse pituitary tumour cell line (AtT20/D16). Interleukin-1β (IL-1β) stimulated production of NO2−/NO3− (NOx) in a time-dependent manner and both NOx and cyclic GMP formation were stimulated in a dose-dependent manner by IL-1β. IL-1β-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-l-arginine (LNMMA), whose effect was reversed by l-arginine, but not by d-arginine. Dexamethasone inhibited IL-1β-induced NOx production in a dose-dependent manner. A calmodulin inhibitor (W-7) showed no effect on IL-1β-induced NOx production, whereas cycloheximide and the actinomycin D completely inhibited NOx production. Northern blot analysis using cDNA for mouse macrophage-inducible NOS as a probe revealed the expression of inducible NOS mRNA in the cells only after exposure to IL-1β. Although IL-1β stimulated ACTH release from tumour cells, LNMMA failed to affect ACTH release stimulated by IL-1β. These results demonstrate for the first time that a pituitary tumour cell line (AtT20/D16) possesses cytokine-inducible and Ca2+/calmodulin-independent NOS, although NO may not be involved in ACTH release. Journal of Endocrinology (1993) 138, 429–435

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.

scholarly journals A Factor(s) from a Rat Trophoblast Cell Line Inhibits Prolactin Secretion in Vitro and in Vivo1

1993 ◽  
Vol 48 (2) ◽  
pp. 325-332 ◽  
Author(s):  
Hiroshi Tomogane ◽  
Lydia A. Arbogast ◽  
Michael J. Soares ◽  
May C. Robertson ◽  
James L. Voogt
Keyword(s):  
Cell Line ◽  
Prolactin Secretion ◽  
Trophoblast Cell ◽  
Trophoblast Cell Line
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