Stimulatory effect of retinoic acid on GH gene expression: the interaction of retinoic acid and tri-iodothyronine in rat pituitary cells

1990 ◽  
Vol 125 (2) ◽  
pp. 251-256 ◽  
Author(s):  
S. Morita ◽  
K. Matsuo ◽  
M. Tsuruta ◽  
S. Leng ◽  
S. Yamashita ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Specific Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Gh Gene ◽  
Rat Pituitary Cells

ABSTRACT We have previously demonstrated that retinoic acid (RA) as well as thyroid hormone stimulates GH gene expression. To clarify the relationship between the action of RA and thyroid hormone, pituitary-specific gene expression was investigated further in rat pituitary cells. Rat clonal pituitary cells, GH3, were treated with RA with or without tri-iodothyronine (T3) for up to 3 days. After treatment with 10–1000 nmol RA/1 with or without 0·1–10 nmol T3/1, medium was collected for radioimmunoassay and cells were subjected to RNA extraction, and GH and prolactin gene expression was analysed using 32P-labelled rat GH and rat prolactin cDNA probes respectively. The data demonstrated the dose–responsive manner of the stimulatory effects of RA and T3 on GH secretion with T3-depleted media. The action of RA was additive to that of T3 for GH secretion when maximum effective doses of RA or T3 were used. Using dot blot and Northern gel analysis, it was shown that RA increased GH mRNA levels in T3-depleted media, and that this action of RA was additive to that of T3 on the induction of GH mRNA levels. In contrast, neither RA nor T3 stimulated the secretion of prolactin and prolactin mRNA levels in these cells. Our results indicate that RA stimulates GH mRNA increment and GH secretion in T3-depleted media, and that the stimulatory effect of RA is additive to the maximum effective dose of T3. Journal of Endocrinology (1990) 125, 251–256

PACAP 38 regulates prolactin (PRL) and growth hormone (GH) secretion and gene expression in cultured rat pituitary cells

1992 ◽  
Vol 40 (2) ◽  
pp. 289
Author(s):  
L. Zheng ◽  
M. Kazemzadeh ◽  
B. Velkeniers ◽  
A. Vandermeers ◽  
J. Christophe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

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.

Effect of Pituitary Adenylate Cyclase-Activating Polypeptide on GH Gene Expression in Rat Pituitary Cells

2006 ◽  
Vol 805 (1) ◽  
pp. 684-691 ◽  
Author(s):  
YUJIN SHUTO ◽  
ANIKÓ SOMOGYVÁRI-VIGH ◽  
SÁNDOR VIGH ◽  
ICHIJI WAKABAYASHI ◽  
AKIRA ARIMURA
Keyword(s):  
Gene Expression ◽  
Adenylate Cyclase ◽  
Pituitary Cells ◽  
Pituitary Adenylate Cyclase ◽  
Rat Pituitary ◽  
Gh Gene ◽  
Rat Pituitary Cells

scholarly journals CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 558
Author(s):  
ZeWen Yu ◽  
WenZhi Ren ◽  
Tian Wang ◽  
WeiDi Zhang ◽  
ChangJiang Wang ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Sequencing Analysis ◽  
Hormone Regulation ◽  
Gh Secretion ◽  
Qrt Pcr ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT–PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT–PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT–PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.

Inhibition by extracellular Na+ replacement of GRF-induced GH secretion from rat pituitary cells

1988 ◽  
Vol 254 (4) ◽  
pp. E476-E481 ◽  
Author(s):  
M. Kato ◽  
M. A. Hattori ◽  
M. Suzuki
Keyword(s):  
Anterior Pituitary ◽  
Channel Blocker ◽  
Na Channel ◽  
Pituitary Cells ◽  
Ionic Mechanism ◽  
Camp Production ◽  
Normal Medium ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

To further clarify the ionic mechanism of the action of growth hormone (GH)-releasing factor (hGRF) on GH secretion, the involvement of extracellular Na+ was studied in perifused dispersed rat anterior pituitary cells. Replacing extracellular Na+ with mannitol or tris(hydroxymethyl)aminomethane (Tris+) suppressed hGRF- and dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced GH secretion. The peak responses to a 2-min application of 1 nM hGRF were 165.0 +/- 5.6 ng/ml (normal medium, mean +/- SE), 21.2 +/- 1.4 ng/ml (Na+-free, mannitol medium), and 18.0 +/- 1.7 ng/ml (Na+-free, Tris+ medium). GH secretion induced by DBcAMP was also suppressed by Na+ replacement to less than 50% of that in normal medium. However, either 15 or 30 mM KCl-stimulated GH secretion was not markedly affected by replacement of Na+ with either compound. Tetrodotoxin, a voltage-sensitive Na+ channel blocker, had no effect on either hGRF- or excess K+-induced GH secretion. cAMP production by hGRF was not greatly affected by replacing extracellular Na+. Thus extracellular Na+ plays an important role in hGRF-induced GH secretion, especially in the process after cAMP production. The involvement of cAMP-sensitive Na+ channels in hGRF-stimulated GH secretion is discussed.

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

172 IN VITRO EXPOSURE TO XENOESTROGENS INDUCES GROWTH HORMONE TRANSCRIPTION AND RELEASE VIA AN ESTROGEN RECEPTOR-DEPENDENT PATHWAY IN RAT PITUITARY GH3 CELLS

2008 ◽  
Vol 20 (1) ◽  
pp. 166
Author(s):  
V.-H. Dang ◽  
E.-B. Jeung
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Estrogen Receptor ◽  
Gene Transcription ◽  
Gh3 Cells ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
In Vitro Exposure ◽  
Gh Gene

The term endocrine disruptor (ED) has been used widely to characterize natural and synthetic environmental compounds that may interfere with the endocrine system(s) of humans and wildlife. In previous studies, we demonstrated that in vitro single exposure to EDs induces CaBP-9k expression, a useful biomarker for detecting the estrogenic activities of EDs in rat pituitary GH3 cells. Here we employ the identical model to examine the effects of EDs in the regulation of growth hormone (GH) gene expression, an important hormone in growth, development, and body composition. We measured levels of GH mRNA transcription and GH release using semi-quantitative RT-PCR and EIA kit, respectively. GH3 cells were treated with alkyphenols (APs), i.e., octyl-phenol (OP), nonyl-phenol (NP), and bisphenol A (BPA), in a dose-dependent manner (10–5, 10–6, and 10–7 M) and harvested following 24 h of treatment. Cells were also exposed to a high concentration (10–5 M) of OP, NP, or BPA and harvested at various time points (1, 3, 6, 12, and 24 h). An anti-estrogen, ICI 182780 (10–7 M) was used to examine the potential involvement of estrogen receptor (ER) in the induction of GH by EDs through an ER-mediated pathway. The data were analyzed by one-way ANOVA, followed by Tukey's multiple comparison. OP, NP, and BPA induced a significant increase in GH gene expression at high (10–5 M) and medium (10–6 M) doses at 24 h. ED-exposure induced a marked increase in GH gene transcription as early as 6 h and peaked at 12 h. Co-treatment with ICI 182780 significantly attenuated ED-induced GH expression in GH3 cells. Interestingly, the level of in vitro GH release was increased significantly at 24 h in response to OP, NP, or BPA, whereas co-treatment with ICI 182780 significantly diminished ED-induced GH secretion in GH3 cells, indicating that ER may play a part in both GH gene transcription and GH release in these cells. Here we demonstrate for the first time that single in vitro exposure to OP, NP, or BPA results in an increase in GH expression at 24 h in GH3 rat pituitary cells. These results may provide new insight into the mode of ED action in GH gene regulation as well as the biological pathway underlying these molecular events. Furthermore, data showing GH responsiveness evoked by EDs supports the aim to develop an assay for use in predicting adverse health effects of EDs in humans and wildlife.

scholarly journals Effect of retinoid status on α, β and γ retinoic acid receptor mRNA levels in various rat tissues

1992 ◽  
Vol 286 (3) ◽  
pp. 755-760 ◽  
Author(s):  
S Kato ◽  
H Mano ◽  
T Kumazawa ◽  
Y Yoshizawa ◽  
R Kojima ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Vitamin A ◽  
Retinoic Acid Receptor ◽  
Rat Tissues ◽  
Mrna Levels ◽  
Acid Receptor ◽  
Beta Gene

We have investigated the effects of retinoids, vitamin D and thyroid hormone on the levels of retinoic acid receptor (RAR)alpha, RAR beta and RAR gamma mRNAs in intact animals. Although vitamin A deficiency caused no significant changes in the levels of RAR alpha and RAR gamma mRNAs, the level of RAR beta transcripts was greatly decreased in various tissues of vitamin A-deficient rats, but was restored rapidly to a normal level after administration of retinoic acid. Retinol also restored the RAR beta mRNA level, but the magnitude and kinetics of the induction differed from those by retinoic acid. The use of specific inhibitors demonstrated that this autoregulation of RAR beta gene expression in vivo occurred at the transcriptional level. In addition, from these results it was postulated that the maintenance of the normal RAR beta mRNA levels seemed to require a threshold serum retinol concentration (about 25 micrograms/dl). Moreover, we found that administration of retinol and retinoic acid to normal rats caused the overexpression of RAR beta transcripts (2-15-fold) when compared with the control levels of RAR beta mRNA, although the levels of RAR alpha and RAR gamma mRNAs were not affected. Vitamin D and thyroid hormone did not modulate the levels of RAR transcripts. These findings clearly indicate the specific ligand regulation of RAR beta gene expression in intact animals. The altered levels of RAR beta according to retinoid status may affect retinoid-inducible gene expression.

Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells

2007 ◽  
Vol 292 (6) ◽  
pp. E1750-E1762 ◽  
Author(s):  
Xinyan Wang ◽  
Mable M. S. Chu ◽  
Anderson O. L. Wong
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Adenylate Cyclase ◽  
Grass Carp ◽  
Promoter Activity ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Gh Gene

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a potent growth hormone (GH)-releasing factor in lower vertebrates. However, its functional interactions with other GH regulators have not been fully characterized. In fish models, norepinephrine (NE) inhibits GH release at the pituitary cell level, but its effects on GH synthesis have yet to be determined. We examined adrenergic inhibition of PACAP-induced GH secretion and GH gene expression using grass carp pituitary cells as a cell model. Through activation of pituitary α2-adrenoreceptors, NE or the α2-agonist clonidine reduced both basal and PACAP-induced GH release and GH mRNA expression. In carp pituitary cells, clonidine also suppressed cAMP production and intracellular Ca2+ levels and blocked PACAP induction of these two second messenger signals. In GH3 cells transfected with a reporter carrying the grass carp GH promoter, PACAP stimulation increased GH promoter activity, and this stimulatory effect could be abolished by NE treatment. In parallel experiments, clonidine reduced GH primary transcript and GH promoter activity without affecting GH mRNA stability, and these inhibitory actions were mimicked by inhibiting adenylate cyclase (AC), blocking protein kinase A (PKA), removing extracellular Ca2+ in the culture medium, or inactivating L-type voltage-sensitive Ca2+ channels (VSCC). Since our recent studies have shown that PACAP can induce GH secretion in carp pituitary cells through cAMP/PKA- and Ca2+/calmodulin-dependent mechanisms, these results, taken together, suggest that α2-adrenergic stimulation in the carp pituitary may inhibit PACAP-induced GH release and GH gene transcription by blocking the AC/cAMP/PKA pathway and Ca2+ entry through L-type VSCC.

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