Somatostatin inhibition of anterior pituitary adenylate cyclase activity: different sensitivity between male and female rats

Schettini, Gennaro; Florio, Tullio; Meucci, Olimpia; Landolfi, E.; Lombardi, Gaetano; Marino, A

doi:10.1016/0006-8993(88)91489-8

Cited by 29 publications

(11 citation statements)

References 17 publications

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“…Specifically, we found that female mice were indeed significantly less sensitive to the inhibitory actions of SST compared with males (Fig. 2), a response similar to that observed in primary PIT cultures prepared from rats (44,53). However, future studies using different doses of SST would need to be performed to unequivocally ascertain whether the observed differences between sexes are related to a change in sensitivity (ED 50 ) and/or in the number of receptors (B max ).…”

Section: Resultssupporting

confidence: 70%

Somatostatin and its receptors contribute in a tissue-specific manner to the sex-dependent metabolic (fed/fasting) control of growth hormone axis in mice

Córdoba-Chacón

Gahete

Castaño

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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Córdoba-Chacón J, Gahete MD, Castaño JP, Kineman RD, Luque RM. Somatostatin and its receptors contribute in a tissuespecific manner to the sex-dependent metabolic (fed/fasting) control of growth hormone axis in mice. Am J Physiol Endocrinol Metab 300: E46 -E54, 2011. First published October 13, 2010; doi:10.1152/ajpendo.00514.2010.-Somatostatin (SST) inhibits growth hormone (GH) secretion and regulates multiple processes by signaling through its receptors sst1-5. Differential expression of SST/ssts may contribute to sex-specific GH pattern and fastinginduced GH rise. To further delineate the tissue-specific roles of SST and sst1-5 in these processes, their expression patterns were evaluated in hypothalamus, pituitary, and stomach of male and female mice under fed/fasted conditions in the presence (wild type) or absence (SST-knockout) of endogenous SST. Under fed conditions, hypothalamic/stomach SST/ssts expression did not differ between sexes, whereas male pituitary expressed more SST and sst2A/2B/3/5A/ 5TMD2/5TMD1 and less sst1, and male pituitary cell cultures were more responsive to SST inhibitory actions on GH release compared with females. This suggests that local pituitary SST/ssts can contribute to the sexually dimorphic pattern of GH release. Fasting (48 h) reduced stomach sst2A/B and hypothalamic SST/sst2A expression in both sexes, whereas it caused a generalized downregulation of pituitary sst subtypes in male and of sst2A only in females. Thus, fasting can reduce SST sensitivity across tissues and SST input to the pituitary, thereby jointly contributing to enhance GH release. In SST-knockout mice, lack of SST differentially altered sst subtype expression levels in both sexes, supporting an important role for SST in sex-dependent control of GH axis. Evaluation of SST, IGF-I, and glucocorticoid effects on hypothalamic and pituitary cell cultures revealed that these hormones could directly account for alterations in sst2/5 expression in the physiological states examined. Taken together, these results indicate that changes in SST output and sensitivity can contribute critically to precisely define, in a tissue-dependent manner, the sex-specific metabolic regulation of the GH axis.

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Section: Resultssupporting

confidence: 70%

Somatostatin and its receptors contribute in a tissue-specific manner to the sex-dependent metabolic (fed/fasting) control of growth hormone axis in mice

Córdoba-Chacón

Gahete

Castaño

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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“…Normal rat hypothalami and anterior pituitaries were isolated from adult male Wistar rats (Charles River Italica, Calco, Italy) as reported previously (Schettini et al, 1988(Schettini et al, , 1989. Total RNA was isolated from rat brain samples and GH4C1 cells using the acid phenol extraction.…”

Section: Methodsmentioning

confidence: 99%

Chemokine Stromal Cell-Derived Factor 1α Induces Proliferation and Growth Hormone Release in GH4C1 Rat Pituitary Adenoma Cell Line through Multiple Intracellular Signals

Florio¹,

Casagrande²,

Diana³

et al. 2005

Mol Pharmacol

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We used GH4C1 cells as a model to study the effects of the chemokine stromal cell-derived factor 1 (SDF1) in pituitary functions. In these cells, SDF1␣ induced proliferation and growth hormone secretion, suggesting a possible regulatory role for this chemokine at pituitary level. We evaluated the intracellular signaling involved in these effects: SDF1␣ increased cytosolic [Ca 2ϩ ] and activated Pyk2, extracellular signal-regulated kinases 1 and 2 (ERK1/2), and large-conductance Ca 2ϩ -activated K ϩ channels (BK Ca ) channels. To correlate these intracellular effectors with the proliferative and secretory effects, we inhibited their activity using BAPTA-AM (Ca 2ϩ chelator), 2Ј-amino-3Ј-methoxyflavone (PD98059; a mitogen-activated protein kinase kinase inhibitor), salicylate (Pyk2 inhibitor), and tetraethyl ammonium (K ϩ channel blocker). All of these compounds reverted SDF1␣-induced proliferation, suggesting the involvement of multiple intracellular pathways. Conversely, only BAPTA-AM reverted growth hormone secretion. To identify a possible cross-talk and a molecular ordering among these pathways, we tested these antagonists on SDF1␣-dependent activation of ERK1/2, Pyk2, and BK Ca channels. From these experiments, we observed that the inhibition of [Ca 2ϩ ] i increase or BK Ca channel activity did not affect ERK1/2 activation by SDF1␣; Pyk2 activation was purely Ca 2ϩ -dependent, not involving ERK1/2 or BK Ca channels; and BK Ca channel activity was antagonized by Pyk2 but not by ERK1/2 inhibitors. These data suggest that an SDF1␣-dependent increase of [Ca 2ϩ ] i activates Pyk2, which in turn regulates BK Ca channel activity. Conversely, ERK1/2 activation is an independent phenomenon.In conclusion, we demonstrate that SDF1␣ causes both proliferation and growth hormone release from pituitary adenoma cells, suggesting that the activation of CXCR4 may represent a novel regulatory mechanism for growth hormone secretion and pituitary cell proliferation, which may contribute to pituitary adenoma development.

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“…In many different cell types, including pituitary and brain, which represent two major somatostatin targets, somatostatin is able to reduce basal and stimulated cAMP production, acting through a G i -protein to reduce the AC activity (Dorflinger & Schonbrunn 1983, Schettini et al 1988b.…”

Section: Intracellular Signalling Of Endogenous Somatostatin Receptorsmentioning

confidence: 99%

Multiple intracellular effectors modulate physiological functions of the cloned somatostatin receptors

Florio¹,

Schettini²

1996

Journal of Molecular Endocrinology

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Somatostatin inhibition of anterior pituitary adenylate cyclase activity: different sensitivity between male and female rats

Cited by 29 publications

References 17 publications

Somatostatin and its receptors contribute in a tissue-specific manner to the sex-dependent metabolic (fed/fasting) control of growth hormone axis in mice

Somatostatin and its receptors contribute in a tissue-specific manner to the sex-dependent metabolic (fed/fasting) control of growth hormone axis in mice

Chemokine Stromal Cell-Derived Factor 1α Induces Proliferation and Growth Hormone Release in GH4C1 Rat Pituitary Adenoma Cell Line through Multiple Intracellular Signals

Multiple intracellular effectors modulate physiological functions of the cloned somatostatin receptors

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