Dexamethasone control of growth hormone mRNA levels in GH3 pituitary cells is cycloheximide-sensitive and primarily posttranscriptional

1989 ◽  
Vol 66 (1) ◽  
pp. 71-82 ◽  
Author(s):  
Jeannine S. Strobl ◽  
Guillaume J.J.M. van Eys ◽  
E.Brad Thompson
Keyword(s):  
Growth Hormone ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Growth Hormone Mrna

scholarly journals Endogenous retinoid X receptors can function as hormone receptors in pituitary cells.

1994 ◽  
Vol 14 (11) ◽  
pp. 7105-7110 ◽  
Author(s):  
K D Davis ◽  
T J Berrodin ◽  
J E Stelmach ◽  
J D Winkler ◽  
M A Lazar
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Ligand Binding ◽  
Hormone Receptors ◽  
Nuclear Hormone Receptors ◽  
Growth Hormone Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Retinoid X Receptors ◽  
X Receptors

Retinoids regulate gene transcription by interacting with both retinoic acid (RA) receptors (RARs) and retinoid X receptors (RXRs). Since unliganded RXRs can act as heterodimerization partners for RARs and other nuclear hormone receptors, it is unclear whether ligand binding by RXRs actually regulates the expression of naturally occurring genes. To address this issue, we synthesized the RXR-selective retinoid SR11237 and confirmed its specificity in transient transfection and proteolytic susceptibility assays before using it to assess the contribution of ligand-activated RXRs to retinoid action. Unlike RAR ligands, SR11237 did not increase endogenous RAR beta mRNA levels in F9 embryonal carcinoma cells, even though it activated transcription of an RXR-responsive reporter gene in these cells. Thus, it is likely that RARs mediate the induction of RAR beta gene expression by RA. In contrast, the RXR-specific ligand induced rat growth hormone mRNA in GH3 pituitary cells, indicating that the effects of RA on growth hormone gene expression at least in part involve ligand binding to endogenous RXRs in vivo. Our results indicate that in addition to serving as cofactors for other nuclear hormone receptors, endogenous RXRs can function as ligand-dependent regulators of gene expression, i.e., classical nuclear hormone receptors.

PKC and ERK are differentially involved in gonadotropin-releasing hormone-induced growth hormone gene expression in the goldfish pituitary

2005 ◽  
Vol 289 (6) ◽  
pp. R1625-R1633 ◽  
Author(s):  
Christian Klausen ◽  
Takeshi Tsuchiya ◽  
John P. Chang ◽  
Hamid R. Habibi
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Primary Cultures ◽  
Gonadotropin Releasing Hormone ◽  
Growth Hormone Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Gh Gene

Gonadotropin-releasing hormone (GnRH) is produced by the hypothalamus and stimulates the synthesis and secretion of gonadotropin hormones. In addition, GnRH also stimulates the production and secretion of growth hormone (GH) in some fish species and in humans with certain clinical disorders. In the goldfish pituitary, GH secretion and gene expression are regulated by two endogenous forms of GnRH known as salmon GnRH and chicken GnRH-II. It is well established that PKC mediates GnRH-stimulated GH secretion in the goldfish pituitary. In contrast, the signal transduction of GnRH-induced GH gene expression has not been elucidated in any model system. In this study, we demonstrate, for the first time, the presence of novel and atypical PKC isoforms in the pituitary of a fish. Moreover, our results indicate that conventional PKCα is present selectively in GH-producing cells. Treatment of primary cultures of dispersed goldfish pituitary cells with PKC activators (phorbol ester or diacylglycerol analog) did not affect basal or GnRH-induced GH mRNA levels, and two different inhibitors of PKC (calphostin C and GF109203X) did not reduce the effects of GnRH on GH gene expression. Together, these results suggest that, in contrast to secretion, conventional and novel PKCs are not involved in GnRH-stimulated increases in GH mRNA levels in the goldfish pituitary. Instead, PD98059 inhibited GnRH-induced GH gene expression, suggesting that the ERK signaling pathway is involved. The results presented here provide novel insights into the functional specificity of GnRH-induced signaling and the regulation of GH gene expression.

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

scholarly journals Association of a PIT1 gene polymorphism with growth hormone mRNA levels in pig pituitary glands

2005 ◽  
Vol 28 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Maurício Machaim Franco ◽  
Robson Carlos Antunes ◽  
Katiana Mello de Oliveira ◽  
Cícero Donizete Pereira ◽  
Fernando Henrique Biase ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gene Polymorphism ◽  
Mrna Levels ◽  
Growth Hormone Mrna ◽  
Pituitary Glands

Endogenous retinoid X receptors can function as hormone receptors in pituitary cells

1994 ◽  
Vol 14 (11) ◽  
pp. 7105-7110
Author(s):  
K D Davis ◽  
T J Berrodin ◽  
J E Stelmach ◽  
J D Winkler ◽  
M A Lazar
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Ligand Binding ◽  
Hormone Receptors ◽  
Nuclear Hormone Receptors ◽  
Growth Hormone Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Retinoid X Receptors ◽  
X Receptors

Retinoids regulate gene transcription by interacting with both retinoic acid (RA) receptors (RARs) and retinoid X receptors (RXRs). Since unliganded RXRs can act as heterodimerization partners for RARs and other nuclear hormone receptors, it is unclear whether ligand binding by RXRs actually regulates the expression of naturally occurring genes. To address this issue, we synthesized the RXR-selective retinoid SR11237 and confirmed its specificity in transient transfection and proteolytic susceptibility assays before using it to assess the contribution of ligand-activated RXRs to retinoid action. Unlike RAR ligands, SR11237 did not increase endogenous RAR beta mRNA levels in F9 embryonal carcinoma cells, even though it activated transcription of an RXR-responsive reporter gene in these cells. Thus, it is likely that RARs mediate the induction of RAR beta gene expression by RA. In contrast, the RXR-specific ligand induced rat growth hormone mRNA in GH3 pituitary cells, indicating that the effects of RA on growth hormone gene expression at least in part involve ligand binding to endogenous RXRs in vivo. Our results indicate that in addition to serving as cofactors for other nuclear hormone receptors, endogenous RXRs can function as ligand-dependent regulators of gene expression, i.e., classical nuclear hormone receptors.

Time- and dose-related effects of gonadotropin-releasing hormone on growth hormone and gonadotropin subunit gene expression in the goldfish pituitary

2002 ◽  
Vol 80 (9) ◽  
pp. 915-924 ◽  
Author(s):  
Christian Klausen ◽  
John P Chang ◽  
Hamid R Habibi
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Molecular Forms ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Induced Responses ◽  
Releasing Hormone ◽  
Significant Difference

The goldfish brain contains two molecular forms of gonadotropin-releasing hormone (GnRH): salmon GnRH (sGnRH) and chicken GnRH-II (cGnRH-II). In a preliminary report, we demonstrated the stimulation of gonadotropin hormone (GtH) subunit and growth hormone (GH) mRNA levels by a single dose of GnRH at a single time point in the goldfish pituitary. Here we extend the work and demonstrate time- and dose-related effects of sGnRH and cGnRH-II on GtH subunit and GH gene expression in vivo and in vitro. The present study demonstrates important differences between the time- and dose-related effects of sGnRH and cGnRH-II on GtH subunit and GH mRNA levels. Using primary cultures of dispersed pituitary cells, the minimal effective dose of cGnRH-II required to stimulate GtH subunit mRNA levels was found to be 10-fold lower than that of sGnRH. In addition, the magnitudes of the increases in GtH subunit and GH mRNA levels stimulated by cGnRH-II were found to be higher than the sGnRH-induced responses. However, no significant difference was observed between sGnRH and cGnRH-II-induced responses in vivo. Time-related studies also revealed significant differences between sGnRH- and cGnRH-II-induced production of GtH subunit and GH mRNA in the goldfish pituitary. In general, the present study provides novel information on time- and dose-related effects of sGnRH and cGnRH-II on GtH subunit and GH mRNA levels and provides a framework for further investigation of GnRH mechanisms of action in the goldfish pituitary.Key words: gonadotropin-releasing hormone, gonadotropin hormone, growth hormone, gene expression, goldfish.

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