Phorbol ester pretreatment attenuates the growth hormone (GH) response to GH-releasing factor in cultured rat pituitary cells

1988 ◽  
Vol 118 (3) ◽  
pp. 423-428 ◽  
Author(s):  
E. Ohmura ◽  
M. Okada ◽  
Y. Ohba ◽  
N. Onoda ◽  
T. Sano ◽  
...  
Keyword(s):  
Phorbol Ester ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Complete Suppression ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Prolonged Culture ◽  
Subsequent Exposure ◽  
Rat Pituitary Cells ◽  
Cells Cultured

ABSTRACT The effect of phorbol ester pretreatment on rat (r) GH release induced by GH-releasing factor (GRF) or 8-bromo-cyclic (c)AMP was investigated using rat pituitary cells cultured in monolayers. Pretreatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 h significantly suppressed the rGH release induced by GRF, but not that by 8-bromo-cAMP 20 h later; this suppressive effect of TPA was concentration-dependent from 8 to 160 nmol/l, and complete suppression was observed after pretreatment with 80–160 nmol TPA/l. Production of cAMP by pituitary cells stimulated with GRF was similarly attenuated in TPA-pretreated cells. The rGH responsiveness to GRF of these cells was fully recovered on prolonged culture (40 h), suggesting that the inhibitory effect of TPA is reversible. In contrast, pretreatment with GRF (5 nmol/l) resulted in suppression of the rGH response to subsequent exposure to GRF (5 nmol/l) or 8-bromo-cAMP (10 mmol/l), but not to TPA. These observations suggest that pretreatment with TPA modifies the rGH response to GRF at steps before the formation of cAMP. J. Endocr. (1988) 118, 423–428

Effect of phorbol esters on the release of growth hormone and prolactin from rat pituitary cells cultured in monolayer

1984 ◽  
Vol 107 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Eiji Ohmura ◽  
Toshio Tsushima ◽  
Hitomi Murakami ◽  
Kae Wakai ◽  
Kazuo Shizume
Keyword(s):  
Growth Hormone ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Time Course ◽  
Phorbol Esters ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Cells Cultured

Abstract. The effect of phorbol diester tumour promoters on the release of growth hormone (GH) and prolactin (Prl) was studied in rat pituitary cells cultured in monolayer. 12-O-tetradecanoyl phorbol-13-acetate (TPA), the most potent phorbol ester, stimulated GH accumulation in the cultured medium in a dose-dependent manner. TPA also stimulated Prl accumulation. A time course study indicated that TPA mainly stimulates release of GH. The maximal stimulation of GH release by TPA (100 ng/ml) was 3–4-fold over control. Phorbol-12,13-dibutyrate (PDB), another tumour-promoting phorbol ester, stimulated GH release to an extent similar to that of TPA, while a biologically inactive compound, phorbol-12,13-diacetate (PDA), had no effect. TPA-stimulated GH release was not affected by the presence of indomethacin, an inhibitor of prostaglandin (PG) synthesis, indicating that PG is not involved in the process of TPA-stimulated GH release. Co++, a competitive antagonist of Ca++, at 2.0 mm completely suppressed the GH release induced by TPA, and this inhibition was partially reversed by the addition of 2.0 mm Ca++. Verapamil, a Ca++ channel blocker, reduced TPA-stimulated GH release, and trifluoperazine, an inhibitor of Ca-calmodulin formation, had a similar effect. Somatostatin (SRIF) also inhibited the GH release by TPA. These observations are compatible with the idea that Ca++ may be involved in the process of TPA-stimulated GH release. Since TPA has been reported to activate a Ca++- and phospholipiddependent protein kinase (protein kinase C), it is possible that TPA stimulate GH release by activating the enzyme. Further studies are required to clarify this point.

scholarly journals CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 558
Author(s):  
ZeWen Yu ◽  
WenZhi Ren ◽  
Tian Wang ◽  
WeiDi Zhang ◽  
ChangJiang Wang ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Sequencing Analysis ◽  
Hormone Regulation ◽  
Gh Secretion ◽  
Qrt Pcr ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT–PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT–PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT–PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.

Studies on the Conditions Determining the Inhibitory Effect of Somatostatin on Adrenocorticotropin, Prolactin and Thyrotropin Release by Cultured Rat Pituitary Cells

1989 ◽  
Vol 50 (1) ◽  
pp. 44-50 ◽  
Author(s):  
Steven W. Lamberts ◽  
Joke Zuyderwijk ◽  
Fred den Holder ◽  
Peter van Koetsveld ◽  
Leo Hofland
Keyword(s):  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

Inhibitory effect of the uterus on plasma and pituitary FSH in rats

1990 ◽  
Vol 124 (2) ◽  
pp. 183-189 ◽  
Author(s):  
J. C. Biro ◽  
P. Eneroth
Keyword(s):  
Molecular Weight ◽  
Chromatographic Analysis ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Inhibitory Response ◽  
Pituitary Cells ◽  
Pregnant Rats ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

ABSTRACT Plasma concentrations of FSH and LH were measured in ovariectomized, ovohysterectomized, hysterectomized and sham-operated adult, non-pregnant rats at 3, 14, 21 and 28 days after operation. From day 21 after the operation onwards, there were higher concentrations of FSH in plasma in ovohysterectomized than in ovariectomized animals. The concentration of LH was not influenced by hysterectomy. The inhibitory response of FSH and LH to a single dose of oestradiol was not altered by any of the operations. By 2 weeks after surgery, pituitary FSH content had increased in ovohysterectomized animals compared with ovariectomized ones, but this difference was eliminated when ovohysterectomized animals were treated with crude uterine extract. Pituitary contents of LH and prolactin were not influenced by hysterectomy or by treatment with uterine extract, thus indicating the specificity of an inhibitory effect of the uterus on FSH levels. Treatment of hysterectomized and intact animals with uterine extract resulted in a reduction in the weight of the ovaries of 23–38% (P<0·05), indirectly showing the presence of an FSH-inhibiting substance in the extract. Fractionated uterine extract inhibited FSH synthesis by rat pituitary cells in vitro, but had no effect on LH synthesis. Chromatographic analysis indicated that the FSH-inhibiting substance in the uterus has a molecular weight of 10 000–20 000. Journal of Endocrinology (1990) 124, 183–189

Extracellular ATP as an autocrine/paracrine regulator of prolactin release

1997 ◽  
Vol 272 (6) ◽  
pp. E1117-E1123 ◽  
Author(s):  
L. Nunez ◽  
C. Villalobos ◽  
L. S. Frawley
Keyword(s):  
Secretory Granules ◽  
Extracellular Atp ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Cells Cultured ◽  
Local Regulator

Recent evidence demonstrates that ATP, costored with a number of hormones and neurotransmitters in secretory granules, is coreleased during exocytosis of these agents. Here, we explored the possibility that extracellular ATP subserves an autocrine and/or paracrine role in the regulation of prolactin (PRL) release by subjecting rat pituitary cells to various experimental manipulations aimed at evaluating putative interactions between ATP and mammotropes. Our results strongly support the view that ATP functions as a local regulator of PRL secretion. To be more specific, we observed that ATP is released in a predictable manner by physiologically relevant secretagogues that are reasonably targeted to mammotropes. Moreover, we found that ATP can act directly on pituitary cells to stimulate the release of PRL from most (if not all) mammotropes. Finally, we determined that antagonism or removal of ATP leads to a diminution of PRL export from pituitary cells cultured under basal or thyrotropin-releasing hormone-stimulated conditions. On the basis of these results, we propose that ATP acts locally to amplify and prolong the PRL secretory response elicited by a more traditional hypophysiotropic signal.

Effects of a novel gonadotropin-releasing hormone antagonist (ORG 30850) on gonadotropin and prolactin secretion by rat pituitary cells in culture

1991 ◽  
Vol 124 (1) ◽  
pp. 98-106 ◽  
Author(s):  
Paul Franchimont ◽  
Sabine M. Almer ◽  
Chantal-J. Charlet-Renard ◽  
Christine L. Daubresse ◽  
Peter P. Kicovic
Keyword(s):  
Culture Medium ◽  
Gnrh Antagonist ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Pituitary Cells ◽  
Cell Content ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Lh Secretion

Abstract. The effect of a new GnRH antagonist (ORG 30850 ANT) on FSH, LH, and PRL secretion was studied using male rat pituitary cells in monolayer cell culture. In the absence of GnRH, ORG 30850 ANT did not alter spontaneous FSH and LH secretion into culture medium or the cell content of these hormones. In the presence of GnRH (10−8 mol/l), ORG 30850 ANT significantly and dose-dependently inhibited FSH and LH secretion into culture medium while increasing their cell content. Conversely, in the presence of a single dose of ORG 30850 ANT, FSH and LH secretion rose significantly when subjected to increasing amounts of GnRH, whereas the hormonal cell content diminished. Furthermore, inhibition of GnRH-induced FSH and LH release by ORG 30850 ANT was not changed by pre-incubation with the GnRH antagonist regardless of the pre-incubation time. The inhibitory effect of the GnRH antagonist was observed early, with its peak occurring within 6 h of culture. These short-term studies indicate that ORG 30850 ANT specifically inhibits GnRH-induced gonadotropin release into culture medium, exerts no effect on the rate of gonadotropin production in the presence or absence of GnRH, competitively and reversibly inhibits the binding of natural GnRH to its receptors, and does not lead to any modifications in PRL secretion.

Effects of metabolic inhibitors on hormone release, cyclic AMP levels, and oxygen consumption in rat pituitary cells in culture

1987 ◽  
Vol 115 (1) ◽  
pp. 96-104
Author(s):  
Kjersti Sletholt ◽  
Claes Magnusson ◽  
Egil Haug ◽  
Kaare M. Gautvik
Keyword(s):  
Oxygen Consumption ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Metabolic Inhibitors ◽  
Pituitary Cells ◽  
Antimycin A ◽  
Hormone Release ◽  
Calmodulin Antagonist ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

Abstract. The metabolic inhibitors antimycin A (2 μmol/l), dinitrophenol (0.5 mmol/l), and iodoacetate (6 mmol/l) were tested for their effects on hormone release, cAMP levels, and oxygen consumption in clonal strains of rat pituitary cells (GH3 cells). Basal release of growth hormone (GH) and prolactin (PRL) was reduced by all three inhibitors, and thyrotropin-releasing hormone (TRH) (l μmol/l) and K+ (50 mmol/l) stimulated hormone release were blocked. Trifluoperazine, a calmodulin antagonist, inhibited basal GH and PRL release at concentrations up to 30 μmol/l and stimulated above 50 μmol/l. The stimulatory effect of 80 μmol/l trifluoperazine on basal hormone release was eliminated by antimycin A, dinitrophenol, and iodoacetate, whereas the inhibitory effect of antimycin A, dinitrophenol and iodoacetate on basal hormone was not affected by 30 μmol/l trifluoperazine. None of the inhibitors had any effect on the level of cellular cAMP (i.e. intracellular plus extracellular). Oxygen consumption of GH3 cells was blocked by antimycin A, reduced by 25% by iodoacetate and increased by about 100% by dinitrophenol. In contrast, hormone secretion stimulated by TRH and K+ was not accompanied by any measurable alteration in oxygen consumption. Trifluoperazine (⩾ 80 μmol/l) reduced the basal oxygen consumption and blocked the stimulatory effect of dinitrophenol on oxygen consumption. In conclusion, inhibition of the energy generation of GH and PRL-producing cells severely affects the action of secretagogues, although stimulated hormone secretion may not be accompanied by any measurable increase in oygen consumption. The cellular energy supporting hormone secretion is mostly generated via oxidative phosphorylation.

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