scholarly journals Evidence for Ah Receptor Mediation of Increased ACTH Concentrations in Primary Cultures of Rat Anterior Pituitary Cells Exposed to TCDD

1998 ◽  
Vol 46 (2) ◽  
pp. 294-299 ◽  
Author(s):  
Lorelle L. Bestervelt ◽  
Jeff A. Pitt ◽  
Walter N. Piper
Keyword(s):  
Anterior Pituitary ◽  
Primary Cultures ◽  
Ah Receptor ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells

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.

Effect of insulin-like growth factor 1 on gonadotropin release from the hypothalamus-pituitary axis in vitro

1991 ◽  
Vol 125 (2) ◽  
pp. 227-233 ◽  
Author(s):  
Toyokazu Kanematsu ◽  
Minoru Irahara ◽  
Toshikazu Miyake ◽  
Keiji Shitsukawa ◽  
Toshihiro Aono
Keyword(s):  
Growth Factor ◽  
Anterior Pituitary ◽  
Primary Cultures ◽  
Pituitary Cells ◽  
Insulin Like Growth Factor ◽  
Gonadotropin Release ◽  
Anterior Pituitary Cells ◽  
Igf I ◽  
Lh Release ◽  
Perifusion System

Abstract. The effects of insulin-like growth factor-I on gonadotropin release were studied using primary culture of rat anterior pituitary cells incubated with IGF-I (20-5000 μg/l) and a hypothalamus-pituitary perifusion system, in which either the mediobasal hypothalamus-pituitary unit or the pituitary were perifused with IGF-I (20-2000 μg/l). In primary cultures of rat anterior pituitary cells, IGF-I (2000 μg/l) caused a significant increase in the release of both LH (46% increase) and FSH (27% increase). It also caused a significant decrease in the cellular content of LH (9%) and FSH (19%). Its effects in stimulating gonadotropin release were suppressed by administration of anti IGF-I receptor antibody (1 mg/l). In the perifusion system, IGF-I (2000 μg/l) did not affect the LH release from the hypothalamus-pituitary or pituitary alone. However, it caused a significant increase in the GnRH (10−9 mol/l) stimulated LH release from perifused pituitary. These data suggest that IGF-I enhances pituitary gonadotropin release via the IGF-I receptor, but its effect on the hypothalamus was not confirmed.

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