The effects of dopamine on prolactin mRNA levels in rat pituitary cells in culture

1992 ◽  
Vol 70 (3) ◽  
pp. 403-407 ◽  
Author(s):  
Seon H. Shin ◽  
John S. Elce
Keyword(s):  
Ascorbic Acid ◽  
Messenger Rna ◽  
Control Group ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Cells In Culture ◽  
Cell Extracts ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Prolactin Mrna

Dopamine is known to be the prolactin-release inhibiting factor, but the effects of dopamine itself on regulation of prolactin messenger RNA have been little studied because of the instability of dopamine. We have compared the effects of dopamine and bromocriptine on the levels of prolactin mRNA and on the rates of synthesis, storage, and release of prolactin in primary cultured rat pituitary cells. The cells were incubated for 72 h with no secretagogue (control group) or in the presence of either dopamine (10 μmol/L) plus ascorbic acid (100 μmol/L) or bromocriptine (0.1 μmol/L). Prolactin mRNA was measured in cell extracts by means of slot blots, and newly synthesized prolactin was measured in similar incubations by the addition of [3H]leucine, followed by gel electrophoresis. The levels of total prolactin were measured by radioimmunoassay. Prolactin mRNA was reduced to 78 ± 9% (mean ± SEM) of control levels in bromocriptine-treated cells and to 59 ± 7% in dopamine-treated cells, demonstrating that dopamine stabilized by ascorbic acid was able to reduce the levels of prolactin mRNA in rat pituitary cells in culture. Dopamine may act at sites in addition to the dopaminergic D2 receptor, since the level of prolactin mRNA was reduced more by a supramaximal dose of dopamine than by a supramaximal dose of bromocriptine. The results of the [3H]prolactin and prolactin measurements suggested that availability of mRNA was not a major factor in controlling the rate of prolactin synthesis.Key words: prolactin, dopamine, bromocriptine, prolactin mRNA, prolactin biosynthesis, cell culture.

Tri-iodothyronine and phenytoin reduce prolactin messenger RNA levels in cultured rat pituitary cells

1986 ◽  
Vol 109 (3) ◽  
pp. 359-364 ◽  
Author(s):  
J. R. E. Davis ◽  
T. C. Lynam ◽  
J. A. Franklyn ◽  
K. Docherty ◽  
M. C. Sheppard
Keyword(s):  
Gene Transcription ◽  
Messenger Rna ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Prolactin Release ◽  
Dot Hybridization ◽  
Prolactin Gene ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Prolactin Mrna

ABSTRACT Thyroid hormones may regulate prolactin gene transcription. We have previously found that phenytoin inhibits tri-iodothyronine (T3) nuclear binding, and have suggested that phenytoin may act as a partial T3 agonist. We have therefore investigated the effects of phenytoin and T3 on prolactin release and gene transcription, using the technique of cytoplasmic dot hybridization with complementary DNA probes to estimate prolactin messenger (m) RNA concentrations in cytoplasm from cultured rat pituitary cells. Tri-iodothyronine treatment led to a small but significant fall in prolactin release by 72 h, but caused marked dose- and time-dependent reductions in prolactin mRNA levels at 48–72 h. Phenytoin, however, caused more rapid falls in both prolactin release and mRNA concentrations. Neither T3 nor phenytoin significantly altered GH mRNA levels. These studies suggest effects of phenytoin similar, but not identical, to those of T3 in the lactotroph. J. Endocr. (1986) 109, 359–364

Cyclic adenosine nucleotides and growth hormone-releasing factor increase cytosolic growth hormone messenger RNA levels in cultured rat pituitary cells

1986 ◽  
Vol 110 (1) ◽  
pp. 51-57 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey ◽  
S. D. Abbot ◽  
A. Detta ◽  
K. Docherty
Keyword(s):  
Growth Hormone ◽  
Gene Transcription ◽  
Messenger Rna ◽  
Primary Cultures ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Rat Pituitary ◽  
Cdna Hybridization ◽  
Adenosine Nucleotides ◽  
Rat Pituitary Cells

ABSTRACT The cellular mechanisms involved in GH biosynthesis have been investigated by the measurement of steady-state levels of cytosolic GH messenger RNA (mRNA) in primary cultures of rat pituitary cells using an RNA–complementary DNA (cDNA) hybridization assay. Growth hormone mRNA–cDNA hybridization increased in a linear manner with increasing cytosol concentration. Cellular GH mRNA levels rose by an average of 2·4-fold (range, 1·6–3·3; n = five experiments) after exposure to GH-ieleasing factor (GRF(1–40); 10 nmol/l) for 3 days. Treatment with GRF increased the release of GH into the culture medium, and depleted the cellular GH content by 40%. Total GH (in the medium plus cells) after GRF treatment increased by between 1·5- and 3·8-fold, a magnitude similar to the increase in GH mRNA levels. Treatment of cells with dibutyryl adenosine 3′:5′-cyclic monophosphate (1 mmol/l) or forskolin (5 μmol/l) increased the levels of cytosolic GH mRNA by between 1·6- and 4·7-fold. These agents increased GH release into the medium, depleted cellular GH content and increased total GH in the system to the same extent as GRF (10 nmol/l). These data demonstrate that cyclic adenosine nucleotides may mediate the GRF induction of GH gene transcription. In addition, we have shown that increases in the levels of cellular GH mRNA are reflected by increased GH biosynthesis, suggesting that the regulation of hormone gene transcription is one cellular site for the control of hormone biosynthesis and, ultimately, hormone available for release. J. Endocr. (1986) 110, 51–57

Progesterone together with estradiol promotes luteinizing hormone β-subunit mRNA stability in rat pituitary cells cultured in vitro

1996 ◽  
Vol 134 (2) ◽  
pp. 236-242 ◽  
Author(s):  
Deokbae Park ◽  
Minseok cheon ◽  
Changmee Kim ◽  
Kyungjin Kim ◽  
Kyungza Ryu
Keyword(s):  
Mrna Stability ◽  
Actinomycin D ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Ovarian Steroids ◽  
Subunit Mrna ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells

Park D, Cheon M, Kim C, Kim K, Ryu K. Progesterone together with estradiol promotes luteinizing hormoneβ-subunit mRNA stability in rat pituitary cells in vitro. Eur J Endocrinol 1996;134:236–42. ISSN 0804–4643 The present study examined the role of ovarian steroids, estradiol and/or progesterone in the regulation of luteinizing hormone β-subunit (LH-β) mRNA levels and LH release in the rat anterior pituitary cells cultured in vitro. When estradiol (10 nmol/l and/or progesterone (100 nmol/l) were added to the cultures, neither estradiol or progesterone nor both together altered the basal LH-β mRNA levels or LH release. Continuous exposure to gonadotropin-releasing hormone (GnRH, 0.2 nmol/l) for 24 h markedly induced LH-β mRNA accumulation, and in this experimental condition, progesterone alone and progesterone + estradiol further augmented GnRH-induced LH-β mRNA levels and LH release. Then we explored further the possibility that ovarian steroids are involved in modulating LH-β mRNA stability in cultured rat pituitary cells where transcription was inhibited by actinomycin D. Anterior pituitary cells were preincubated with GnRH (0.2 nmol/l) for 16 h and, after removing GnRH from culture medium, the cells were incubated further in the presence of actinomycin D (5 μmol/l) for 24 h. The LH-β mRNA levels gradually declined to about 30% of the control values (zero time point after GnRH removal) in a time-dependent manner. During this period, either progesterone alone or progesterone + estradiol clearly blocked the degradation of LH-β mRNA species. These results indicate that ovarian steroids promote LH-β mRNA stability, thereby contributing to the maintenance of GnRH-stimulated LH-β mRNA levels. Kyungza Ryu, Department of Pharmacology, College of Medicine, Yonsei University, 120-749, Seoul, Korea

Control of the production of two protein hormones by rat pituitary cells in culture

In Vitro ◽  
1970 ◽  
Vol 6 (3) ◽  
pp. 180-189 ◽  
Author(s):  
Frank C. Bancroft ◽  
Armen H. Tashjian
Keyword(s):  
Pituitary Cells ◽  
Cells In Culture ◽  
Rat Pituitary ◽  
Rat Pituitary Cells
Sign in / Sign up

Export Citation Format

Share Document