Poly (adenosine diphosphate-ribose) synthesis in the anterior pituitary of the female rat throughout the estrous cycle: Study of possible relation to cell proliferation and prolactin gene expression

1993 ◽  
Vol 16 (7) ◽  
pp. 475-480 ◽  
Author(s):  
Nobuhiko Suganuma ◽  
F. Kikkawa ◽  
H. Seo ◽  
N. Matsui ◽  
Y. Tomoda
Endocrine ◽  
1999 ◽  
Vol 11 (3) ◽  
pp. 251-256 ◽  
Author(s):  
Jianwei Ren ◽  
James I. Koenig ◽  
Shing C. Hooi

2007 ◽  
Vol 192 (2) ◽  
pp. 429-442 ◽  
Author(s):  
Evelyn Davies ◽  
Selma Omer ◽  
John F Morris ◽  
Helen C Christian

Annexin 1 (ANXA1) is a Ca2+- and phospholipid-binding protein that plays an important role as a mediator of glucocorticoid action in the host-defence and neuroendocrine systems. Sex differences in hypothalamo–pituitary–adrenal (HPA) axis activity are well documented and a number of studies have demonstrated that gonadal steroids act as regulators of HPA activity. The aim of this study was to investigate the effect of ovariectomyand 17β-estradiol replacement, and estrous cycle stage, on anterior pituitary ANXA1 content. The amount of anterior pituitary ANXA1 determined by western blotting varied with estrous cycle stage with a peak at estrus declining to a trough at proestrus. Ovariectomy resulted in a significant (P<0.05) decrease in anterior pituitary ANXA1 content. Administration of 17β-estradiol (1 μg/100 g) significantly (P<0.01) increased anterior pituitary ANXA1 expression in the ovariectomized animals. In contrast, there was no change in pituitary ANXA1 content in response to 17β-estradiol in adrenalectomized and adrenalectomized/ovariectomized rats. Treatment of TtT/GF cells, a folliculo-stellate cell line, with 17β-estradiol (1.8–180 nM) increased ANXA1 mRNA expression and increased the amount of ANXA1 protein externalized in response to a dexamethasone stimulus. These results indicate that 17β-estradiol stimulates ANXA1 expression in the anterior pituitary and in vivo an adrenal factor contributes to the mechanism of action.


1988 ◽  
Vol 14 (4) ◽  
pp. 263-282 ◽  
Author(s):  
Jerome M. Goldman ◽  
Ralph L. Cooper ◽  
Georgia L. Rehnberg ◽  
Kimberly C. Booth ◽  
W. Keith McElroy ◽  
...  

1995 ◽  
Vol 7 (3) ◽  
pp. 225-231 ◽  
Author(s):  
Marie-Noëlle Montagne ◽  
Monique Dussaillant ◽  
Li-Jin Chew ◽  
Anne Berod ◽  
Steven J. Lamberts ◽  
...  

Endocrinology ◽  
1997 ◽  
Vol 138 (4) ◽  
pp. 1374-1384 ◽  
Author(s):  
Rossella E. Nappi ◽  
Serge Rivest

Abstract The purpose of this study was to investigate the influence of immune (systemic endotoxin administration) and metabolic (fasting) challenges on LHRH neuronal activity and transcription in the organum vasculosum of the lamina terminalis/medial preoptic area as well as on the expression of the LHRH receptor (LHRH-R) in the anterior pituitary of cycling female rats. The reproductive stages of adult female rats (200–250 g; 14 h of light; lights on at 0600 h) were verified by daily vaginal smears taken every morning for a minimum of three or four cycles before the experiment. The acute-phase response was induced via an ip injection of lipopolysaccharide (LPS; 200μ g/100 g BW), whereas the metabolic challenge consisted of food deprivation for at least 48 h. Control and challenged rats were killed at specific times in the ovulatory cycle (1200, 1500, and 1800 h on proestrus and diestrous day 2). Frozen brains and pituitaries were mounted on a microtome, cut into 30-μm slices, and then processed for the detection of transcripts encoding either LHRH or LHRH-R by means of in situ hybridization histochemistry using intronic (heteronuclear RNA) and exonic [messenger RNA (mRNA)] riboprobes. Dual immunocytochemistry to detect Fos-immunoreactive (ir) nuclei in LHRH-ir perikarya and colocalization of LHRH mRNA with Fos protein during the day of proestrus were performed by using both in situ hybridization and immunocytochemistry techniques on the same brain sections. The percentage of LHRH-ir and LHRH-expressing neurons displaying positive Fos-ir nuclei during the afternoon of proestrus was significantly inhibited 3 h after endotoxin administration. Rats exhibited an increase in the levels of LHRH primary transcript in the organum vasculosum of the lamina terminalis/medial preoptic area structure at 1500 h on proestrus, a phenomenon significantly attenuated by LPS injection only at this phase of the estrous cycle. On the other hand, fasting did not affect LHRH neuronal activity or gene expression in intact cycling rats, but affected these cells in animals exhibiting a disruption of the ovulatory cycle. Interestingly, LPS caused a profound down-regulation of LHRH-R gene expression in the anterior pituitary throughout the entire estrous cycle. Although food deprivation provoked a more variable pattern of LHRH-R mRNA in cycling rats, the signal for this transcript in the adenohypophysis was deeply altered in those showing a perturbed cycle. These results provide evidence that immune challenge interferes with the LHRH system at both hypothalamic and pituitary levels, whereas alteration of that neuroendocrine system in food-deprived rats seems highly associated with the impairment of reproductive cyclicity.


2001 ◽  
pp. 659-665 ◽  
Author(s):  
SN De Biasi ◽  
LI Apfelbaum ◽  
ME Apfelbaum

OBJECTIVE: The purpose of this work was to study the direct effect of leptin on LH release by anterior pituitary glands from female rats at the time of spontaneous and steroid-induced LH surge. METHODS: LH responsiveness to leptin by pituitaries from rats killed in the afternoon (1500 h) at different stages of the 4-day estrous cycle (diestrus-1: D1; diestrus-2: D2; proestrus; estrus), ovariectomized (OVX; 15 days post-castration) and ovariectomized steroid-primed (OVX-E(2)/Pg; pretreated with 5 microg estradiol and 1 mg progesterone), was evaluated in vitro. Hemi-adenohypophyses were incubated in the presence of synthetic murine leptin for 3 h. RESULTS: Addition of increasing concentrations of leptin (0.1-100 nmol/l) to the incubation medium of proestrus pituitaries produced a dose-related stimulation of LH release; the maximal increase to 315% of control was obtained with 10 nmol/l leptin. Leptin (10 nmol/l) enhanced LH release at all days of the estrous cycle, the greatest response occurring in proestrus (318%) and the lowest at D1 (123%). In order to evaluate the role of nitric oxide (NO) in the action of leptin on LH release, glands from proestrus rats were incubated in the presence of 10 nmol/l leptin with or without 0.3 mmol/l N(G)-monomethyl-l-arginine (NMMA), a competitive inhibitor of NO synthase (NOS). NMMA completely suppressed the stimulation of LH release induced by leptin. Leptin also stimulated LH release by pituitaries from OVX rats, and treatment with steroid hormones led to a marked increase in the response (OVX: 162% compared with OVX-E(2)/Pg: 263%; P<0.05). For comparative analysis, a similar experimental procedure was carried out using GnRH (10 nmol/l). Leptin acts at the pituitary level in a similar manner as GnRH, although with significantly lower potency. CONCLUSIONS: These results confirm and extend previous reports regarding a direct action of leptin at the pituitary level, stimulating LH release by anterior pituitaries from female rats at the time of spontaneous and steroid-induced LH surge. In the female rat pituitary this leptin action is controlled by gonadal steroids and mediated by NO.


Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2164-2171 ◽  
Author(s):  
Yong Qing Wang ◽  
Ren Yuan ◽  
Ya-Ping Sun ◽  
Tae-Jin Lee ◽  
Girish V. Shah

Calcitonin-like pituitary peptide, which is synthesized and secreted by gonadotrophs of the rat anterior pituitary (AP) gland, is a potent inhibitor of prolactin biosynthesis and lactotroph cell proliferation. Because TGF-β1 is an autocrine inhibitor of lactotroph cell proliferation, we investigated a possibility that calcitonin (CT) interacts with TGF-β1 to inhibit lactotroph cell proliferation. The actions of CT on GGH3 cell proliferation were examined in the absence or presence of anti-TGF-β1 serum. Subsequent experiments tested the effects of CT on TGF-β1 mRNA abundance as well as TGF-β1 synthesis. The studies also tested whether the stimulatory action of CT on TGF-β1 mRNA expression involves stabilization of TGF-β1 mRNA. Finally, the experiments investigated in vivo actions of CT on TGF-β1 synthesis in the AP gland. This was accomplished by studying the changes induced by iv administered CT in TGF-β1-immunopositive cell populations of adult female rat AP glands. The results have shown that the inhibitory action of CT on proliferation of GGH3 cells was attenuated by rabbit anti-TGF-β1 serum. Moreover, CT stimulated TGF-β1 mRNA expression, as well as TGF-β1 synthesis, in a dose-dependent fashion. Stimulatory action of CT on TGF-β1 expression may be posttranscriptional, because it significantly increased TGF-β1 mRNA stability. When administered in vivo, CT significantly increased TGF-β1-immunopositive cell populations of adult female rat AP gland. Colocalization studies for prolactin and TGF-β1 suggest that CT increased TGF-β1 synthesis in lactotrophs, and possibly in nonlactotroph cell populations. These results suggest that antiproliferative action of CT on lactotrophs may, at least in part, be mediated by CT-induced TGF-β1 expression.


1995 ◽  
Vol 132 (6) ◽  
pp. 771-776 ◽  
Author(s):  
Byung J Lee ◽  
Jin H Kim ◽  
Chae K Lee ◽  
Hae M Kang ◽  
Hyun C Kim ◽  
...  

Lee BJ, Kim JH, Lee CK, Kang HM, Kim HC, Kang SG. Changes in mRNA levels of a pituitary-specific trans-acting factor, Pit-1, and prolactin during the rat estrous cycle. Eur J Endocrinol 1995;132:771–6. ISSN 0804–4643 The present study examined the changes in mRNA levels of a pituitary-specific trans-acting factor, Pit-1, and prolactin during the rat estrous cycle. Total cytoplasmic RNA was analyzed by Northern blot and slot-blot hybridization to examine the prolactin mRNA level. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to examine the Pit-1 mRNA level. Proestrous and estrous prolactin mRNA levels were significantly higher than the metestrous and diestrous levels, whereas Pit-1 mRNA levels of the estrous and metestrous stages were about two- to threefold higher than those of the proestrous and diestrous stages. Proestrous Pit-1 mRNA levels increased gradually from 10.00 h to 20.00 h, while prolactin mRNA levels slightly decreased until 14.00 h but increased later until 20.00 h. During the rat estrous cycle, especially in the afternoon of the proestrous day, changes of prolactin mRNA levels seem to follow a prior increase of Pit-1 mRNA. Therefore, Pit-1 may be partly involved in the regulation of prolactin gene expression according to the rat estrous cycle. Estradiol administration to ovariectomized rats significantly increased both the mRNA levels of prolactin and Pit-1, which suggests that the gene expression of Pit-1 is regulated by estrogen through indirect extracellular pathways. Byung Ju Lee, Department of Biology, College of Natural Sciences, University of Ulsan 680-749, Ulsan, South Korea


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