Tachykinins and their gene expression in the anterior pituitary of the siberian hamster—Effects of photoperiod, thyroid hormones, and analogs of hypothalamic hormones

Endocrine ◽  
1995 ◽  
Vol 3 (11) ◽  
pp. 839-843 ◽  
Author(s):  
L. Debeljuk ◽  
J. N. Rao ◽  
A. Bartke
Keyword(s):  
Gene Expression ◽  
Thyroid Hormones ◽  
Anterior Pituitary ◽  
Siberian Hamster ◽  
Hypothalamic Hormones

Galanin gene expression in radiothyroidectomy-induced thyrotroph adenomas

1996 ◽  
Vol 271 (1) ◽  
pp. E24-E30
Author(s):  
J. F. Hyde ◽  
J. P. Moore ◽  
K. W. Drake ◽  
D. G. Morrison
Keyword(s):  
Gene Expression ◽  
Thyroid Hormones ◽  
Anterior Pituitary ◽  
Human Growth ◽  
Mrna Levels ◽  
Male Mice ◽  
Pituitary Glands ◽  
Positive Regulators ◽  
Hypothalamic Pituitary Axis ◽  
Iodine 131

Galanin gene expression is markedly increased in the anterior pituitary glands of estrogen-treated rats (lactotroph hyperplasia) as well as human growth hormone-releasing hormone transgenic mice (somatotroph hyperplasia). The objective of this study was to examine galanin in a mouse model of thyrotroph adenoma formation. Male mice were radiothyroidectomized by use of iodine-131 (131I), and galanin peptide levels were assessed in the hypothalamic-pituitary axis. Immunoreactive galanin concentrations in the anterior pituitaries of 131I-treated mice were decreased 80% at 3, 6, 9, and 12 mo after radiothyroidectomy. Galanin peptide levels in the hypothalamus were decreased 20-25% at these times. Treatment with either estradiol or 3,3',5-triiodo-L-thyronine increased galanin peptide concentrations in the anterior pituitaries of 131I-treated mice, but neither treatment restored galanin concentrations. Galanin mRNA levels were decreased > 80% 1 yr after radiothyroidectomy. We conclude that, unlike animal models of lactotroph and somatotroph hyperplasia, galanin gene expression is suppressed throughout the development of thyrotroph adenomas, suggesting that galanin does not have a stimulatory role in the proliferation of thyrotrophs. Moreover, these data show that thyroid hormones are important positive regulators of galanin gene expression in the mouse and that estrogen may stimulate galanin gene expression in the absence of thyroid hormones.

Evidence of thyrotropin-releasing hormone (TRH) gene expression in rat anterior pituitaries and modulation by estrogens of TRH-like immunoreactivity and TRH-elongated peptide contents

1996 ◽  
Vol 151 (1) ◽  
pp. 87-96 ◽  
Author(s):  
G Croissandeau ◽  
N Schussler ◽  
D Grouselle ◽  
P Pagesy ◽  
C Rauch ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Hormones ◽  
Anterior Pituitary ◽  
Cross Reactivity ◽  
Plasma Prolactin ◽  
Ovx Rats ◽  
First Time ◽  
Intact Rats

Abstract TRH gene expression in the anterior pituitary has previously been reported in the human in vivo and in the rat in vitro. Until now, modulation of this synthesis with glucocorticoids and thyroid hormones has been observed in rats. The present study demonstrates for the first time that the TRH gene is also expressed, in vivo, in the rat anterior pituitary and that anterior pituitary TRH-like immunoreactivity (TRH-LI) and elongated forms of the immediate TRH progenitor sequence (TRH-elongated peptide) contents are also modulated by estrogens (E2). To investigate the presence of proTRH mRNA in the rat anterior pituitary, total RNA was reverse transcribed (RT) and the RT products were then amplified by PCR. Treatments with E2 were performed on intact and ovariectomized (OVX) rats for 2 months. TRH-LI was measured by RIA with an antibody which did not recognize the TRH-like peptide, pGlu-Glu-Pro-NH2 (<EEP-NH2) (cross-reactivity <0·1%) and was characterized further as TRH-LI by HPLC. TRH-elongated peptides were measured by EIA and characterized by Sephadex G-50 chromatography and immunoblotting (molecular mass 25–35 kDa). The plasma prolactin levels and the pituitary sizes were increased by E2 treatment in both intact and OVX rats. Anterior pituitary TRH-LI increased in intact E2-treated rats compared with intact rats (82·7 ± 19·0 versus 39·6 ± 3·6 fmol/mg protein; means ± s.e.m.; P<0·001). This increase was greater when E2 was administered to OVX rats (599·0 ± 98·4 after E2 treatment versus 58·6 ± 3·6 fmol/mg protein; P<0·001). In intact rats, anterior pituitary TRH-elongated peptide contents were not modified by E2 treatment while they were significantly decreased in OVX E2-treated rats (144·6 ±8·8 versus 223·7 ± 9·5 fmol/mg protein; P<0·001). These results demonstrate TRH gene expression in the rat anterior pituitary in vivo and suggest that E2 treatment is responsible for an increase in anterior pituitary TRH-LI, together with a decrease in TRH-elongated peptide contents. Journal of Endocrinology (1996) 151, 87–96

Effect of thyroid hormones on vasoactive intestinal polypeptide gene expression in the rat cerebral cortex and anterior pituitary

1995 ◽  
Vol 55 (3) ◽  
pp. 237-251 ◽  
Author(s):  
Thora Buhl ◽  
Birgitte Georg ◽  
Christer Nilsson ◽  
Jens D. Mikkelsen ◽  
Birgitte S. Wulff ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Thyroid Hormones ◽  
Vasoactive Intestinal Polypeptide ◽  
Anterior Pituitary ◽  
Rat Cerebral Cortex ◽  
Intestinal Polypeptide

P173 effects of tetrahydroisoquinolines on the POMC gene expression in anterior pituitary tumor cells

1994 ◽  
Vol 2 (1-2) ◽  
pp. 162
Author(s):  
I. Putscher ◽  
H. Haber ◽  
J. Fickel ◽  
A. Winkler ◽  
M. Melzig
Keyword(s):  
Gene Expression ◽  
Tumor Cells ◽  
Pituitary Tumor ◽  
Anterior Pituitary ◽  
Pomc Gene

scholarly journals Hesx1 homeodomain protein represses transcription as a monomer and antagonises transactivation of specific sites as a homodimer

2002 ◽  
Vol 28 (3) ◽  
pp. 193-205 ◽  
Author(s):  
J Quirk ◽  
P Brown
Keyword(s):  
Gene Expression ◽  
Dna Binding ◽  
Binding Site ◽  
Anterior Pituitary ◽  
Homeodomain Protein ◽  
Dependent Manner ◽  
Gene Promoters ◽  
Differentiation Markers ◽  
Proximal Half ◽  
Dna Binding Site

The homeobox repressor Hesx1, expressed throughout Rathke's pouch and required for normal pituitary development, has been implicated in anterior pituitary pathogenesis in man. Prolonged expression of Hesx1 delays the appearance of anterior pituitary terminal differentiation markers in mice, particularly the gonadotroph hormones. We tested if Hesx1 could modulate gonadotrophin gene expression directly, and found that Hesx1 repressed both common alpha subunit (alpha GSU) and luteinising hormone beta-subunit (LH beta) gene promoters. Repression mapped to the Pitx1 homeodomain protein transactivation site in the proximal alpha GSU promoter, but did not map to the equivalent site on LH beta. Hesx1 repression of the alpha GSU Pitx1 site was overridden by co-transfection of Pitx1. In contrast, Hesx1 antagonised Pitx1 transactivation of LH beta in a dose-dependent manner. This was due to monomeric binding of Hesx1 on alpha GSU and homodimerisation on LH beta. The homodimerisation site comprises the Pitx1 DNA binding site and a proximal binding site, and mutation of either inhibited homodimer formation. Conversion of the LH beta Pitx1 DNA binding site to an alpha GSU-type did not promote homodimer formation, arguing that Hesx1 has pronounced site selectivity. Furthermore, mutation of the proximal half of the homodimerisation site blocked Hesx1 antagonisation of Pitx1 transactivation. We conclude that Hesx1 monomers repress gene expression, and homodimers block specific transactivation sites.

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