Time-Specific Effects of Perinatal Glucocorticoid Treatment on Anterior Pituitary Morphology, Annexin 1 Expression and Adrenocorticotrophic Hormone Secretion in the Adult Female Rat

2006 ◽  
Vol 18 (12) ◽  
pp. 949-959 ◽  
Author(s):  
C. D. John ◽  
E. Theogaraj ◽  
H. C. Christian ◽  
J. F. Morris ◽  
S. F. Smith ◽  
...  
Keyword(s):  
Adult Female ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Female Rat ◽  
Adrenocorticotrophic Hormone ◽  
Glucocorticoid Treatment ◽  
Annexin 1 ◽  
Specific Effects ◽  
Time Specific

scholarly journals The influence of 17β-estradiol on annexin 1 expression in the anterior pituitary of the female rat and in a folliculo-stellate cell line

2007 ◽  
Vol 192 (2) ◽  
pp. 429-442 ◽  
Author(s):  
Evelyn Davies ◽  
Selma Omer ◽  
John F Morris ◽  
Helen C Christian
Keyword(s):  
Cell Line ◽  
Estrous Cycle ◽  
Anterior Pituitary ◽  
Stellate Cell ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Annexin 1 ◽  
17Β Estradiol ◽  
Estrous Cycle Stage

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.

scholarly journals Antiproliferative Action of Calcitonin on Lactotrophs of the Rat Anterior Pituitary Gland: Evidence for the Involvement of Transforming Growth Factor β1 in Calcitonin Action

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2164-2171 ◽  
Author(s):  
Yong Qing Wang ◽  
Ren Yuan ◽  
Ya-Ping Sun ◽  
Tae-Jin Lee ◽  
Girish V. Shah
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Adult Female ◽  
Anterior Pituitary ◽  
Cell Populations ◽  
Female Rat ◽  
Stimulatory Action ◽  
Immunopositive Cell ◽  
Tgf Β1

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.

scholarly journals Effect of neonatal and adult testosterone treatment on the cellular composition of the adult female rat anterior pituitary

2000 ◽  
Vol 164 (3) ◽  
pp. 265-276 ◽  
Author(s):  
S Gonzazalez-Parra ◽  
J Argente ◽  
LM Garcia-Segura ◽  
JA Chowen
Keyword(s):  
Adult Female ◽  
Anterior Pituitary ◽  
Neonatal Period ◽  
Female Rats ◽  
Pituitary Hormone ◽  
Mrna Levels ◽  
Female Rat ◽  
Cellular Composition ◽  
Testosterone Treatment ◽  
Silver Grains

The adult female pituitary has significantly more lactotrophs than that of the male, while the later has a higher percent of somatotrophs. It is clear that GH and prolactin (PRL) gene expression and somatotroph and lactotroph proliferation are modulated by the postpubertal hormone environment; however, the role of the neonatal steroid environment in this process is not known. We have used in situ hybridization to determine the number of GH and PRL mRNA-containing cells, as well as the level of expression of these two hormones, in response to neonatal and adult testosterone treatment. Female rats exposed to testosterone during the neonatal period, adulthood or both periods, as well as normal females and males were used. Exposure to testosterone during the neonatal period significantly increased the percentage of somatotrophs (ANOVA: P<0. 005) and decreased that of lactotrophs in the adult female rat (ANOVA: P<0.001). Adult testosterone treatment had no significant effect on the percentage of somatotrophs. The percentage of lactotrophs was significantly increased by adult testosterone only in those rats also exposed to neonatal testosterone. PRL mRNA concentrations, as reflected by silver grains/cell, were reduced by neonatal testosterone and increased by adult testosterone treatment (ANOVA: P<0.0001). Overall PRL mRNA levels, measured by densitometry, were also reduced by neonatal testosterone exposure, but adult testosterone had no effect (ANOVA: P<0.001). GH mRNA levels per cell, as reflected by silver grains/cell, were increased by adult testosterone, while neonatal testosterone treatment had no effect. Overall GH mRNA levels per unit area, determined by densitometry measurements, were increased by both neonatal and adult testosterone treatment, with the combination of these two treatments resulting in adult females having levels indistinguishable from intact males (ANOVA: P<0.003). These results suggest that, in combination with postpubertal sex steroids, the neonatal gonadal steroid environment plays an important role in determining anterior pituitary hormone synthesis and cellular composition.

POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE
Keyword(s):  
Inhibitory Action ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Immature Rat ◽  
Rat Strain ◽  
Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

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