scholarly journals Exocytotic protein components in rat pituitary gland after long-term estrogen administration

1999 ◽  
Vol 161 (2) ◽  
pp. 323-331 ◽  
Author(s):  
G Majo ◽  
MJ Lorenzo ◽  
J Blasi ◽  
F Aguado
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Anterior Pituitary Cells ◽  
Pituitary Glands ◽  
Protein Components

Recently, a set of proteins involved in the docking and fusion machinery of secretory organelles has been identified in anterior pituitary cells. In this study we analyzed, by Western blotting and immunocytochemistry, the expression of several proteins involved in exocytosis after long-term administration of 17beta-estradiol (E2) in Fischer 344 rats. No differences were observed in the amount of synaptosomal-associated protein of 25 kDa, synaptobrevin 2, syntaxin 1, synaptotagmin I and Rab3a in total brain homogenates from treated rats after E2 administration. In striking contrast, the levels of all of these exocytotic proteins, including cellubrevin, were notably decreased in pituitary glands of E2-treated rats. In addition, no differences were observed in the in vitro basal and 8-Br-cAMP-induced prolactin (PRL) release between pituitary cells from control and E2-treated rats, whereas TRH-induced PRL release in anterior pituitary cells from E2-treated animals was higher than in control donors. In conclusion, this study shows that protein components of the exocytotic machinery are specifically down-regulated in the pituitary gland of E2-treated Fischer 344 rats.

scholarly journals Intermedin/Adrenomedullin-2 Inhibits Growth Hormone Release from Cultured, Primary Anterior Pituitary Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 859-864 ◽  
Author(s):  
Meghan M. Taylor ◽  
Sara L. Bagley ◽  
Willis K. Samson
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Prolactin Secretion ◽  
Anterior Pituitary Gland ◽  
Male Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Peptide Family

Intermedin (IMD), a novel member of the adrenomedullin (AM), calcitonin gene-related peptide (CGRP), amylin (AMY) peptide family, has been reported to act promiscuously at all the known receptors for these peptides. Like AM and CGRP, IMD acts in the circulation to decrease blood pressure and in the brain to inhibit food intake, effects that could be explained by activation of the known CGRP, AM, or AMY receptors. Because AM, CGRP, and AMY have been reported to affect hormone secretion from the anterior pituitary gland, we examined the effects of IMD on GH, ACTH, and prolactin secretion from dispersed anterior pituitary cells harvested from adult male rats. IMD, in log molar concentrations ranging from 1.0 pm to 100 nm, failed to significantly alter basal release of the three hormones. Similarly, IMD failed to significantly alter CRH-stimulated ACTH or TRH-stimulated prolactin secretion in vitro. However, IMD concentration-dependently inhibited GHRH-stimulated GH release from these cell cultures. The effects of IMD, although requiring higher concentrations, were as efficacious as those of somatostatin and, like somatostatin, may be mediated, at least in part, by decreasing cAMP accumulation. These actions of IMD were not shared by other members of the AM-CGRP-AMY family of peptides, suggesting the presence of a novel, unique IMD receptor in the anterior pituitary gland and a potential neuroendocrine action of IMD to interact with the hypothalamic mechanisms controlling growth and metabolism.

Interleukin 6 possibly induced by interleukin 1β in the pituitary gland stimulates the release of gonadotropins and prolactin

1990 ◽  
Vol 122 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Masaaki Yamaguchi ◽  
Noboru Matsuzaki ◽  
Kenji Hirota ◽  
Akira Miyake ◽  
Osamu Tanizawa
Keyword(s):  
Pituitary Gland ◽  
Interleukin 6 ◽  
Anterior Pituitary ◽  
Interleukin 1 ◽  
Interleukin 1Β ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

Abstract The abilities of recombinant human interleukin 1 (IL-1) and IL-6 to induce release of FSH, LH and PRL from rat pituitary cells in vitro were examined. IL-1 and IL-6 induced significant releases of FSH, LH and PRL within 3 h. The extents of release of these compounds induced by IL-1 and IL-6 were similar to those induced by GnRH and TRH. Rat anterior pituitary cells released IL-6 spontaneously, and its release was enhanced by IL-1β. This effect of IL-1β was inhibited significantly by a rabbit anti-IL-1β antiserum. These findings suggest that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL-6 stimulated the secretions of FSH, LH and PRL.

Further studies on the regulation, localization and function of the TRH-like peptide pyroglutamyl-glutamyl-prolineamide in the rat anterior pituitary gland

1995 ◽  
Vol 146 (2) ◽  
pp. 293-300 ◽  
Author(s):  
J M M Rondeel ◽  
W Klootwijk ◽  
E Linkels ◽  
P H M Jeucken, W ◽  
L J Hofland ◽  
...  
Keyword(s):  
Body Weight ◽  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Lhrh Antagonist

Abstract Recent evidence shows that thyrotrophin-releasing hormone (TRH) immunoreactivity in the rat anterior pituitary gland is accounted for by the TRH-like tripeptide prolineamide-glutamyl-prolineamide (pGlu-Glu-ProNH2, <EEP-NH2). The present study was undertaken to investigate further the regulation, localization and possible intrapituitary function of <EEP-NH2. Anterior pituitary levels of <EEP-NH2 were determined between days 5 and 35 of life, during the oestrous cycle and after treatment with the luteinizing hormone-releasing hormone (LHRH) antagonist Org 30276. Treatment of adult males with the LHRH antagonist either for 1 day (500 μg/100 g body weight) or for 5 days (50 μg/100 g body weight) reduced anterior pituitary <EEP-NH2 levels by 25–30% (P<0·05 versus saline-treated controls). Anterior pituitary <EEP-NH2 increased between days 5 and 35 of life. In females, these levels were 2- to 3-fold higher (P<0·05) than in males between days 15 and 25 after birth; these changes corresponded with the higher plasma follicle-stimulating hormone (FSH) levels in the female rats. After day 25, <EEP-NH2 levels in female rats decreased in parallel with a decrease in plasma FSH. Injections with the LHRH antagonist (500 μg/100 g body weight), starting on day 22 of life, led to reduced contents of <EEP-NH2 in the anterior pituitary gland of female rats on days 26 and 30 (55 and 35% decrease respectively). Levels of <EEP-NH2 in the anterior pituitary gland did not change significantly during the oestrous cycle. Fractionation of anterior pituitary cells by unit gravity sedimentation was found to be compatible with the localization of <EEP-NH2 in gonadotrophs. In vitro, <EEP-NH2 dose-dependently inhibited TRH-stimulated growth hormone (GH) release from anterior pituitary cells obtained from neonatal rats, but no consistent effects were seen on the in vitro release of luteinizing hormone (LH), FSH, prolactin (PRL) or thyroid-stimulating hormone (TSH) under basal or TRH/LHRH-stimulated conditions. Furthermore, <EEP-NH2 did not affect the in vitro hormone release by anterior pituitary cells obtained from adult rats. In vivo, <EEP-NH2 (0·3–1·0 μg intravenously) did not affect plasma PRL, TSH, LH, FSH and GH in adult male rats. We conclude that <EEP-NH2 in the anterior pituitary gland is regulated by LHRH, is probably localized in gonadotrophs and may play a (paracrine) role in neonatal GH release. Journal of Endocrinology (1995) 146, 293–300

scholarly journals In Vivo and In Vitro Arsenic Exposition Induces Oxidative Stress in Anterior Pituitary Gland

2016 ◽  
Vol 35 (4) ◽  
pp. 463-475 ◽  
Author(s):  
Sonia A. Ronchetti ◽  
María S. Bianchi ◽  
Beatriz H. Duvilanski ◽  
Jimena P. Cabilla
Keyword(s):  
Oxidative Stress ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inorganic Arsenic ◽  
Anterior Pituitary Gland ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Stress Responsive Genes

Inorganic arsenic (iAs) is at the top of toxic metalloids. Inorganic arsenic-contaminated water consumption is one of the greatest environmental health threats worldwide. Human iAs exposure has been associated with cancers of several organs, neurological disorders, and reproductive problems. Nevertheless, there are no reports describing how iAs affects the anterior pituitary gland. The aim of this study was to investigate the mechanisms involved in iAs-mediated anterior pituitary toxicity both in vivo and in vitro. We showed that iAs administration (from 5 to 100 ppm) to male rats through drinking water increased messenger RNA expression of several oxidative stress-responsive genes in the anterior pituitary gland. Serum prolactin levels diminished, whereas luteinizing hormone (LH) levels were only affected at the higher dose tested. In anterior pituitary cells in culture, 25 µmol/L iAs significantly decreased prolactin release in a time-dependent fashion, whereas LH levels remained unaltered. Cell viability was significantly reduced mainly by apoptosis evidenced by morphological and phosphatidylserine externalization studies. This process is characterized by early depolarization of mitochondrial membrane potential and increased levels of reactive oxygen species. Expression of some key oxidative stress-responsive genes, such as heme oxygenase-1 and metallothionein-1, was also stimulated by iAs exposure. The antioxidant N-acetyl cysteine prevented iAs-induced effects on the expression of oxidative stress markers, prolactin release, and apoptosis. In summary, the present work demonstrates for the first time that iAs reduces prolactin release both in vivo and in vitro and induces apoptosis in anterior pituitary cells, possibly resulting from imbalanced cellular redox status.

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

Inhibitory effects of fumagillin and its analogue TNP-470 on the function, morphology and angiogenesis of an oestrogen-induced prolactinoma in Fischer 344 rats

1996 ◽  
Vol 150 (1) ◽  
pp. 99-106 ◽  
Author(s):  
H Stępień ◽  
M Grochal ◽  
K W Zieliński ◽  
S Mucha ◽  
J Kunert-Radek ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Anterior Pituitary ◽  
Angiogenesis Inhibitors ◽  
Prolactin Secretion ◽  
Prolonged Treatment ◽  
Endothelial Cell Proliferation ◽  
Pituitary Cells ◽  
Fischer 344 ◽  
F344 Rats

Abstract The process of angiogenesis occurs in many physiological states, but it is also essential for the growth of solid tumours and metastasis formation. An abnormal arterial vascularization has been shown in prolactin-secreting pituitary adenomas induced by prolonged treatment with oestrogens in Fischer 344 (F344) rats. It is thought that anti-angiogenic agents might be useful in therapy for these tumours. Fumagillin and its analogue TNP-470 are known to inhibit endothelial cell proliferation selectively, but their effect on lactotroph cell secretory function and prolactinoma formation has not yet been described. The aim of the present study was to examine the effects of fumagillin and TNP-470 on prolactin secretion, and morphological and vascular changes within the anterior pituitary in long-term oestrogen-treated male F344 rats in vivo and in vitro. As expected, 7 weeks after s.c. implantation of Silastic tubes containing 10 mg diethylstilboestrol (DES), a very high rise in serum prolactin levels was found. Both angiogenesis inhibitors injected s.c. at doses of 10 mg/kg body weight for 24 days attenuated the stimulatory effect of DES on prolactin production and release. They also diminished prolactin cell density and inhibited cell proliferation expressed as the number of anterior pituitary cells labelled with bromodeoxyuridine (BrdU), but the effect of TNP-470 was minor compared with fumagillin. Both angioinhibitors suppressed neovascularization within the anterior pituitary with similar potency but, on the other hand, they did not affect DES-induced increases in prolactin secretion from cultured rat pituitary cells and cell proliferation in vitro. In conclusion, our results provide strong evidence for the anti-tumour and anti-prolactin activity of angiogenesis inhibitors in the experimentally oestrogen-induced pituitary adenoma; this might be mediated indirectly through the inhibition of angiogenesis. Journal of Endocrinology (1996) 150, 99–106

scholarly journals Cytochemical staining of the endoplasmic reticulum and glycogen in mouse anterior pituitary cells.

1984 ◽  
Vol 32 (12) ◽  
pp. 1285-1294 ◽  
Author(s):  
A M Cataldo ◽  
R D Broadwell
Keyword(s):  
Endoplasmic Reticulum ◽  
Nuclear Envelope ◽  
Anterior Pituitary ◽  
Cell Types ◽  
Pituitary Cells ◽  
Cytochemical Staining ◽  
Anterior Pituitary Cells ◽  
G6pase Activity ◽  
Pituitary Glands ◽  
Glycogen Particles

The endoplasmic reticulum (ER) and glycogen in secretory cells of anterior pituitary glands from control and fasted mice were investigated ultrastructurally using cytochemical staining techniques. Potential enzyme cytochemical markers for the ER included glucose-6-phosphatase (G6Pase) and nucleoside diphosphatase (NDPase) activities. Presumptive glycogen particles were identified in tissue postfixed in 1% osmium tetroxide-1.5% potassium ferrocyanide or in ultrathin sections poststained with periodic acid-thiocarbohydrazide-silver proteinate. The ER appeared to be related structurally and cytochemically to the nuclear envelope and cis Golgi saccules. Similar relationships between the ER and the trans Golgi saccules or GERL were not observed. In anterior pituitary glands from control mice, G6Pase activity was prominent within the lumen of the ER, nuclear envelope, and cis Golgi saccules of all cells; reaction product was absent in the trans Golgi saccules and in GERL. G6Pase activity was sparse to non-existent in anterior pituitary cells from fasted mice. The cytochemical reaction utilizing the Gomori lead capture method indicated that G6Pase in anterior pituitary cells may function as a phosphohydrolase for converting glucose-6-phosphate to glucose. Cytochemical localization of NDPase activity was not evident in the ER; reaction product was localized consistently in one or two trans Golgi saccules and occasionally in GERL and nascent secretory granules. Presumptive glycogen particles in each of the different secretory cell types from control mice appeared as 20-30 nm wide, electron-dense particles scattered as single entities throughout the cytoplasm. Anterior pituitary glands from fasted mice exhibited conspicuous and numerous clumps of glycogen particles in addition to scattered particles in all cell types except corticotrophs, which appeared to be devoid of glycogen. Glycogen particles were absent in anterior pituitary cells incubated in a medium containing diastase. Our results suggest that in anterior pituitary cells of the mouse: 1) the phosphohydrolytic activity of G6Pase is a reliable cytochemical marker for the ER; 2) the ER is associated morphologically and cytochemically with the cis face but not with the trans face of the Golgi apparatus or with GERL; 3) some glucose-6-phosphate, a possible substrate for G6Pase in vivo, may be derived indirectly from glycogen stores; and 4) modulations in G6Pase activity and glycogen storage during fasting may reflect an alteration in energy metabolism.

An in vitro model for studies of intercellular communication in cultured rat anterior pituitary cells

1984 ◽  
Vol 16 (4) ◽  
pp. 483-497 ◽  
Author(s):  
William W. Wilfinger ◽  
William J. Larsen ◽  
Thomas R. Downs ◽  
Donald L. Wilbur
Keyword(s):  
Intercellular Communication ◽  
Anterior Pituitary ◽  
In Vitro Model ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Vitro Model
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