scholarly journals Rat Anterior Pituitary Folliculostellate Cells Are Targets of Interleukin-1β and a Major Source of Intrapituitary Follistatin

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 732-740 ◽  
Author(s):  
Louise M. Bilezikjian ◽  
Angela M. O. Leal ◽  
Amy L. Blount ◽  
Anne Z. Corrigan ◽  
Andrew V. Turnbull ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Cell Function ◽  
Pituitary Hormones ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Mrna Accumulation ◽  
Folliculostellate Cells ◽  
Pituitary Adenylate Cyclase ◽  
Immortalized Cell ◽  
Insight Into

Folliculostellate cells of the anterior pituitary are postulated to be an important source of factors, such as follistatin, that regulate pituitary function by intercellular communication. To gain further insight into the function of this cell type, folliculostellate cells were enriched from cultured rat anterior pituitary cells, and an immortalized cell line designated FS/D1h was established and characterized. These FS/D1h cells express S100 immunoreactivity and produce IL-6 but not pituitary hormones such as GH, ACTH, FSH, and LH. Importantly, FS/D1h cells express large amounts of follistatin mRNA and secrete the protein, as quantified indirectly by the amount of [125I]activin A immunoprecipitated with a follistatin antiserum. The FS/D1h cells also express α, βA, and βB inhibin/activin subunit mRNAs, but whether they produce the corresponding activins and inhibins has not been determined. The response of FS/D1h cells to agents thought to modulate folliculostellate cell function was evaluated. IL-1β (0.005–5 nm) stimulated the secretion of follistatin and increased mRNA expression. In parallel, IL-6 secretion was stimulated. Dexamethasone, pituitary adenylate cyclase-activating polypeptide(1–27), and lipopolysaccharide but not testosterone, 12-O-tetradecanoylphorbol-13-acetate, or forskolin also increased follistatin secretion. Surprisingly, activin had no effect on follistatin mRNA levels, despite the fact that FS/D1h cells express ActRII, ActRIIB, and ALK-4 (ActRIB). Activin, on the other hand, induced Smad7 mRNA accumulation and exerted an antiproliferative effect on FS/D1h cells. Altogether, these observations support the possibility that follistatin originating from folliculostellate cells participates in mediating the effects of IL-1β, glucocorticoids, and other agents on the response of pituitary cells to activins.

scholarly journals Expression and regulation of glucocorticoid-induced leucine zipper in the developing anterior pituitary gland

2008 ◽  
Vol 42 (2) ◽  
pp. 171-183 ◽  
Author(s):  
Laura E Ellestad ◽  
Stefanie A Malkiewicz ◽  
H David Guthrie ◽  
Glenn R Welch ◽  
Tom E Porter
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Leucine Zipper ◽  
Pituitary Hormones ◽  
Neuroendocrine System ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Anterior Pituitary Hormone

The expression profile of glucocorticoid-induced leucine zipper (GILZ) in the anterior pituitary during the second half of embryonic development in the chick is consistent with in vivo regulation by circulating corticosteroids. However, nothing else has been reported about the presence of GILZ in the neuroendocrine system. We sought to characterize expression and regulation of GILZ in the chicken embryonic pituitary gland and determine the effect of GILZ overexpression on anterior pituitary hormone levels. Pituitary GILZ mRNA levels increased during embryogenesis to a maximum on the day of hatch, and decreased through the first week after hatch. GILZ expression was rapidly upregulated by corticosterone in embryonic pituitary cells. To determine whether GILZ regulates hormone gene expression in the developing anterior pituitary, we overexpressed GILZ in embryonic pituitary cells and measured mRNA for the major pituitary hormones. Exogenous GILZ increased prolactin mRNA above basal levels, but not as high as that in corticosterone-treated cells, indicating that GILZ may play a small role in lactotroph differentiation. The largest effect we observed was a twofold increase in FSH β subunit in cells transfected with GILZ but not treated with corticosterone, suggesting that GILZ may positively regulate gonadotroph development in a manner not involving glucocorticoids. In conclusion, this is the first report to characterize avian GILZ and examine its regulation in the developing neuroendocrine system. We have shown that GILZ is upregulated by glucocorticoids in the embryonic pituitary gland and may regulate expression of several pituitary hormones.

scholarly journals Estrogen mediates sex differences in preoptic neuropeptide and pituitary hormone production in medaka

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Junpei Yamashita ◽  
Yuji Nishiike ◽  
Thomas Fleming ◽  
Daichi Kayo ◽  
Kataaki Okubo
Keyword(s):  
Anterior Pituitary ◽  
Pituitary Hormones ◽  
Pituitary Hormone ◽  
Sexually Dimorphic ◽  
Hormone Production ◽  
Anterior Pituitary Hormones ◽  
Vertebrate Brain ◽  
Pituitary Adenylate Cyclase ◽  
Evolutionarily Conserved ◽  
Sexually Dimorphic Expression

AbstractThe preoptic area (POA) is one of the most evolutionarily conserved regions of the vertebrate brain and contains subsets of neuropeptide-expressing neurons. Here we found in the teleost medaka that two neuropeptides belonging to the secretin family, pituitary adenylate cyclase-activating polypeptide (Pacap) and vasoactive intestinal peptide (Vip), exhibit opposite patterns of sexually dimorphic expression in the same population of POA neurons that project to the anterior pituitary: Pacap is male-biased, whereas Vip is female-biased. Estrogen secreted by the ovary in adulthood was found to attenuate Pacap expression and, conversely, stimulate Vip expression in the female POA, thereby establishing and maintaining their opposite sexual dimorphism. Pituitary organ culture experiments demonstrated that both Pacap and Vip can markedly alter the expression of various anterior pituitary hormones. Collectively, these findings show that males and females use alternative preoptic neuropeptides to regulate anterior pituitary hormones as a result of their different estrogen milieu.

scholarly journals IGF-I regulates pro-opiomelanocortin and GH gene expression in the mouse pituitary gland

2003 ◽  
Vol 178 (1) ◽  
pp. 71-82 ◽  
Author(s):  
J Honda ◽  
Y Manabe ◽  
R Matsumura ◽  
S Takeuchi ◽  
S Takahashi
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Northern Blotting ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Gh Treatment ◽  
Gh Receptor ◽  
Pomc Mrna ◽  
Igf I ◽  
Mouse Pituitary

IGF-I is expressed in somatotrophs, and IGF-I receptors are expressed in most somatotrophs and some corticotrophs in the mouse pituitary gland. Our recent study demonstrated that IGF-I stimulates the proliferation of corticotrophs in the mouse pituitary. These results suggested that somatotrophs regulate corticotrophic functions as well as somatotrophic functions by the mediation of IGF-I molecules. The present study aimed to clarify factors regulating pituitary IGF-I expression and also the roles exerted by IGF-I within the mouse anterior pituitary gland. Mouse anterior pituitary cells were isolated and cultured under serum-free conditions. GH (0.5 or 1 microg/ml), ACTH (10(-8) or 10(-7) M), GH-releasing hormone (GHRH; 10(-8) or 10(-7) M), dexamethasone (DEX; 10(-8) or 10(-7) M) and estradiol-17beta (e2; 10(-11) or 10(-9) M) were given for 24 h. IGF-I mRNA levels were measured using competitive RT-PCR, and GH and pro-opiomelanocortin (POMC) mRNA levels were measured using Northern blotting analysis. GH treatment significantly increased IGF-I mRNA levels (1.5- or 2.1-fold). ACTH treatment did not alter GH and IGF-I mRNA levels. IGF-I treatment decreased GH mRNA levels (0.7- or 0.5-fold), but increased POMC mRNA levels (1.8-fold). GH treatment (4 or 8 microg/ml) for 4 days increased POMC mRNA levels. GHRH treatment increased GH mRNA levels (1.3-fold), but not IGF-I mRNA levels. DEX treatment significantly decreased IGF-I mRNA levels (0.8-fold). e2 treatment did not affect IGF-I mRNA levels. GH receptor mRNA, probably with GH-binding protein mRNA, was detected in somatotrophs, and some mammotrophs and gonadotrophs by in situ hybridization using GH receptor cDNA as a probe. These results suggested that IGF-I expression in somatotrophs is regulated by pituitary GH, and that IGF-I suppresses GH expression and stimulates POMC expression at the transcription level. Pituitary IGF-I produced in somatotrophs is probably involved in the regulation of somatotroph and corticotroph functions.

Influence of Calcium Ions on Proopiomelanocortin mRNA Levels in Clonal Anterior Pituitary Cells

1988 ◽  
Vol 47 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Gerhard Von Dreden ◽  
Jean-Philippe Loeffler ◽  
Cornelia Grimm ◽  
Volker Höllt
Keyword(s):  
Calcium Ions ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Anterior Pituitary Cells

Pituitary Disorders

2016 ◽  
pp. 191-202
Author(s):  
Pankaj Shah
Keyword(s):  
Metastatic Disease ◽  
Anterior Pituitary ◽  
Pituitary Tumors ◽  
Pituitary Hormones ◽  
Pituitary Cells ◽  
Pituitary Disease ◽  
Tissue Resistance ◽  
Common Causes ◽  
Sheehan Syndrome ◽  
Pituitary Infarction

Hypopituitarism usually results from a deficiency of anterior pituitary hormones or, rarely, from tissue resistance to these hormones. Deficiency may be from primary pituitary disease, pituitary stalk disorders, hypothalamic disease, or an extrasellar disorder impinging on, or infiltrating, the hypothalamic-pituitary unit. Primary pituitary disease results from the loss of anterior pituitary cells and may be congenital or acquired. Common causes are pituitary tumors and their surgical or radiotherapeutic ablation. Infrequent causes include pituitary infarction (eg, postpartum pituitary necrosis, also known as Sheehan syndrome), pituitary apoplexy, lymphocytic hypophysitis, infiltrative diseases (eg, hemochromatosis), and metastatic disease (eg, from breast or lung).

Tumor necrosis factor-alpha and interferon-gamma reduce prolactin release in vitro

1990 ◽  
Vol 259 (5) ◽  
pp. E672-E676
Author(s):  
P. E. Walton ◽  
M. J. Cronin
Keyword(s):  
Anterior Pituitary ◽  
Tumor Necrosis ◽  
Cell Function ◽  
Tnf Alpha ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Necrosis Factor Alpha ◽  
Ifn Gamma ◽  
Factor Alpha ◽  
Necrosis Factor

Prolactin binds to lymphocytes and monocytes and can modulate immune cell function. It was postulated that proteins released from activated macrophages and lymphocytes could directly influence prolactin release and thus form an endocrine control loop during infection, tumor invasion, or inflammation. This hypothesis was tested by exposing cultured rat anterior pituitary cells to murine tumor necrosis factor-alpha (TNF-alpha) and/or interferon-gamma (IFN-gamma) for 24 h before a 4-h test of cell function. Overall prolactin accumulation during this first 24 h was inhibited by TNF-alpha and markedly reduced by TNF-alpha plus IFN-gamma. In contrast, thyroid-stimulating hormone levels were unchanged in these same media. During the subsequent 4-h challenge, both cytokines reduced thyrotropin-releasing hormone-stimulated prolactin release but had no effect on inhibited prolactin release mediated by dopamine and somatostatin receptors. Cellular viability (assessed by trypan blue and chromium release assays) and prolactin cell content were unchanged after TNF-alpha or IFN-gamma treatment. We conclude that both TNF-alpha and IFN-gamma have the potential to act directly on anterior pituitary cells to slow the rate of prolactin release.

scholarly journals Novel fish hypothalamic neuropeptides stimulate the release of gonadotrophins and growth hormone from the pituitary of sockeye salmon

2006 ◽  
Vol 188 (3) ◽  
pp. 417-423 ◽  
Author(s):  
Masafumi Amano ◽  
Shunsuke Moriyama ◽  
Masayuki Iigo ◽  
Shoji Kitamura ◽  
Noriko Amiya ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Sockeye Salmon ◽  
Brain Regions ◽  
Pituitary Hormones ◽  
Reversed Phase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pituitary Cells ◽  
Reversed Phase Hplc ◽  
Hypothalamic Neuropeptides ◽  
The Brain

We recently identified a cDNA encoding three novel fish hypothalamic neuropeptides, having LPXRF-NH2 from the goldfish brain. In this study, to clarify the physiological functions of these three LPXRFamide peptides (gfLPXRFa-1, -2, and -3), we analysed the localisation and hypophysiotrophic activity of these peptides using sockeye salmon, Oncorhynchus nerka, in which immunoassay systems for several anterior pituitary hormones have been developed. gfLPXRFa-immunoreactive cell bodies were detected in the nucleus posterioris periventricularis of the hypothalamus and immunoreactive fibres were distributed in various brain regions and the pituitary. We also detected gfLPXRFa-immunoreactivity in the pituitary by competitive enzyme-linked immunosorbent assay combined with reversed-phase HPLC. These three gfLPXRFamide peptides stimulated the release of FSH, LH and GH, but did not affect the release of prolactin (PRL) and somatolactin (SL) from cultured pituitary cells. These results suggest that novel fish hypothalamic LPXR-Famide peptides exist in the brain and pituitary of sockeye salmon and stimulate the release of gonadotrophins and GH from the pituitary.

scholarly journals Goldfish Calmodulin: Molecular Cloning, Tissue Distribution, and Regulation of Transcript Expression in Goldfish Pituitary Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5056-5067 ◽  
Author(s):  
Longfei Huo ◽  
Eric K. Y. Lee ◽  
P. C. Leung ◽  
Anderson O. L. Wong
Keyword(s):  
Amino Acid ◽  
Adenylate Cyclase ◽  
Mrna Expression ◽  
Hormone Secretion ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Reading Frame ◽  
Pituitary Adenylate Cyclase ◽  
Neuroendocrine Mechanisms

Abstract Calmodulin (CaM) is a Ca2+-binding protein essential for biological functions mediated through Ca2+-dependent mechanisms. In the goldfish, CaM is involved in the signaling events mediating pituitary hormone secretion induced by hypothalamic factors. However, the structural identity of goldfish CaM has not been established, and the neuroendocrine mechanisms regulating CaM gene expression at the pituitary level are still unknown. Here we cloned the goldfish CaM and tested the hypothesis that pituitary expression of CaM transcripts can be the target of modulation by hypothalamic factors. Three goldfish CaM cDNAs, namely CaM-a, CaM-bS, and CaM-bL, were isolated by library screening. These cDNAs carry a 450-bp open reading frame encoding the same 149-amino acid CaM protein, the amino acid sequence of which is identical with that of mammals, birds, and amphibians and is highly homologous (≥90%) to that in invertebrates. In goldfish pituitary cells, activation of cAMP- or PKC-dependent pathways increased CaM mRNA levels, whereas the opposite was true for induction of Ca2+ entry. Basal levels of CaM mRNA was accentuated by GnRH and pituitary adenylate cyclase-activating polypeptide but suppressed by dopaminergic stimulation. Pharmacological studies using D1 and D2 analogs revealed that dopaminergic inhibition of CaM mRNA expression was mediated through pituitary D2 receptors. At the pituitary level, D2 activation was also effective in blocking GnRH- and pituitary adenylate cyclase-activating polypeptide-stimulated CaM mRNA expression. As a whole, the present study has confirmed that the molecular structure of CaM is highly conserved, and its mRNA expression at the pituitary level can be regulated by interactions among hypothalamic factors.

Sign in / Sign up

Export Citation Format

Share Document