Estradiol stimulates prolactin gene transcription in primary cultures of rat anterior pituitary cells

1987 ◽  
Vol 26 (4) ◽  
pp. 451-456 ◽  
Author(s):  
James D. Shull ◽  
Jane H. Walent ◽  
Jack Gorski
Keyword(s):  
Gene Transcription ◽  
Anterior Pituitary ◽  
Primary Cultures ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Prolactin Gene

scholarly journals Dopaminergic regulation of avian prolactin gene transcription

2003 ◽  
Vol 31 (1) ◽  
pp. 185-196 ◽  
Author(s):  
A Al Kahtane ◽  
Y Chaiseha ◽  
M El Halawani
Keyword(s):  
Gene Expression ◽  
Steady State ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Anterior Pituitary ◽  
Good Evidence ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Steady State Levels ◽  
Prl Gene

It is well documented that prolactin (PRL) release and PRL gene expression in birds are controlled by the tonic stimulation of hypothalamic vasoactive intestinal peptide (VIP). However, there is good evidence that dopamine (DA) exerts both stimulatory (at the hypothalamic level) and inhibitory (at the pituitary level) effects on PRL secretion. The interactions between VIP and DA in the regulation of PRL gene transcription are not known. This study was designed to examine the effects of a D(2) DA receptor agonist (D(2)AG; R(-)-propylnorapomorphine HCl) on basal and VIP-stimulated PRL gene transcription rate, PRL mRNA steady-state levels, PRL mRNA stability and PRL release from cultured turkey anterior pituitary cells. The D(2)AG (10(-)(10) M) completely inhibited the stimulatory effect of VIP (10(-)(7) M) upon nascent PRL mRNA as determined utilizing a nuclear run-on transcription assay. To examine further the effect of the D(2)AG on PRL mRNA post-transcriptional events, anterior pituitary cells were treated with different concentrations of D(2)AG (10(-)(12)-10(-)(4) M). Semi-quantitative RT-PCR and RIA were performed to determine the levels of PRL mRNA and PRL content in the medium respectively. The results show that D(2)AG inhibited VIP-stimulated PRL mRNA steady-state levels as well as basal and VIP-stimulated PRL release, effects which were diminished by the D(2) DA receptor antagonist, S(-)-eticlopride HCl (10(-)(10) M). Actinomycin D (5 microg/ml), an inhibitor of mRNA synthesis, was used to assess the effect of D(2)AG on PRL mRNA stability in response to VIP. The stimulatory effect of VIP on PRL mRNA stability was completely negated by the D(2)AG (from a half-life of 53.0+/-2.3 h in VIP-treated cells to 25.5+/-1.6 h in D(2)AG+VIP-treated cells, P<or=0.05). These results support the hypothesis that VIP and DA play a major role in the regulation of PRL gene expression in avian species, at both the transcriptional and post-transcriptional levels. In addition, these findings suggest that the DAergic system inhibits PRL release and synthesis by antagonizing VIP at the pituitary level via D(2) DA receptors.

Estrogens exert a rapid apoptotic action in anterior pituitary cells

2009 ◽  
Vol 296 (4) ◽  
pp. E664-E671 ◽  
Author(s):  
S. Zárate ◽  
G. Jaita ◽  
V. Zaldivar ◽  
D. B. Radl ◽  
G. Eijo ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Primary Cultures ◽  
Ovariectomized Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Steroid Signaling ◽  
A Cell ◽  
17Β Estradiol ◽  
Induced Apoptosis ◽  
Classical Mechanism

It is now accepted that estrogens not only stimulate lactotrope proliferation but also sensitize anterior pituitary cells to proapoptotic stimuli. In addition to their classical mechanism of action through binding to intracellular estrogen receptors (ERs), there is increasing evidence that estrogens exert rapid actions mediated by cell membrane-localized ERs (mERs). In the present study, we examined the involvement of membrane-initiated steroid signaling in the proapoptotic action of estradiol in primary cultures of anterior pituitary cells from ovariectomized rats by using estren, a synthetic estrogen with no effect on classical transcription and a cell-impermeable 17β-estradiol conjugate (E2-BSA). Both compounds induced cell death of anterior pituitary cells after 60 min of incubation as assessed by flow cytometry and the [3-(4,5-dimethylthiazol-2-yl)]-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Estren, E2, and E2-BSA induced apoptosis of lactotropes and somatotropes as evaluated by the deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay and immunodetection of prolactin (PRL) and growth hormone (GH). The proapoptotic effect of E2-BSA was abrogated by ICI-182,780, an antagonist of ERs. The expression of membrane-associated ERα was observed in PRL- and GH-bearing cells. Our results indicate that estradiol is able to exert a rapid apoptotic action in anterior pituitary cells, especially lactotropes and somatotropes, by a mechanism triggered by mERs. This mechanism could be involved in anterior pituitary cell turnover.

STRIATED MUSCLE FIBERS DIFFERENTIATE IN PRIMARY CULTURES OF ADULT ANTERIOR PITUITARY CELLS

Endocrinology ◽  
1988 ◽  
Vol 122 (6) ◽  
pp. 3002-3004 ◽  
Author(s):  
Ofra Spira ◽  
Ruth Atzmon ◽  
Ezra Rahamim ◽  
Rachel Bar-Shavit ◽  
Jack Gross ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Striated Muscle ◽  
Primary Cultures ◽  
Muscle Fibers ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Striated Muscle Fibers

scholarly journals Effects of Vasopressin V1b Receptor Deficiency on Adrenocorticotropin Release from Anterior Pituitary Cells in Response to Oxytocin Stimulation

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 4883-4891 ◽  
Author(s):  
Kazuaki Nakamura ◽  
Yoko Fujiwara ◽  
Reiko Mizutani ◽  
Atsushi Sanbe ◽  
Noriko Miyauchi ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Receptor Antagonist ◽  
Anterior Pituitary ◽  
Primary Cultures ◽  
Control Level ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
V1b Receptor ◽  
Rat Pituitary ◽  
Acth Release

Oxytocin (OT) is one of the secretagogues for stress-induced ACTH release. OT-induced ACTH release is reported to be mediated by the vasopressin V1b receptor in the rat pituitary gland, which contains both OT and V1b receptors. We examined OT-induced ACTH release using primary cultures of anterior pituitary cells from wild-type (V1bR+/+) and V1b receptor knockout (V1bR−/−) mice. OT stimulated similar levels of ACTH release from pituitary cells of V1bR+/+ and V1bR−/− mice. OT-induced ACTH release was significantly inhibited by the selective V1b receptor antagonist SSR149415 and the OT receptor antagonist CL-14-26 in V1bR+/+ mice. In addition, cotreatment with SSR149415 at 10−6m and CL-14-26 at 10−6m inhibited OT-induced ACTH release to the control level inV1bR+/+ mice. In V1bR−/− mice, OT-induced ACTH release was significantly inhibited by CL-14-26 at 10−8m and completely inhibited at 10−7m. These results indicate that OT induces the ACTH response via OT and V1b receptors inV1bR+/+ mice but via only OT receptors in V1bR−/− mice. The gene expression level of the OT receptor was significantly higher in the anterior pituitary gland of V1bR−/− mice than in that of V1bR+/+ mice, suggesting that the OT receptor is up-regulated to compensate for ACTH release under conditions of V1b receptor deficiency.

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