Nitric oxide stimulates embryonic somatotroph differentiation and growth hormone mRNA and protein expression through a cyclic guanosine monophosphate-independent mechanism

Chen, H.P.; Zhang, L.; Xu, Biao; Kang, Lumei; Shu, Yang; Zeng, Huihong; Shi, Xin

doi:10.1016/j.tice.2008.09.002

Cited by 3 publications

(3 citation statements)

References 40 publications

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“…However, the reported effects of NO are conflicting, with NO described either as inhibitory or stimulatory on gonadotroph cells [17,[39][40][41]. Several lines of evidence suggest that gonadotroph-originating NO may influence the secretory activity of other pituitary endocrine cells such as GnRH INDUCES PITUITARY NOS1 VIA THE PKA PATHWAY somatotropes, lactotropes, and corticotropes [42,43]. Moreover, recent studies [44,45] have highlighted the mediatory role of NOS1 in GnRH modulation of activin-induced or ghrelin-induced gonadotropin synthesis and/or release.…”

Section: Discussionmentioning

confidence: 99%

Sustained Gonadotropin-Releasing Hormone Stimulation Mobilizes the cAMP/PKA Pathway to Induce Nitric Oxide Synthase Type 1 Expression in Rat Pituitary Cells In Vitro and In Vivo at Proestrus1

Garrel

Simon

Thieulant

et al. 2010

Biology of Reproduction

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Previous in vivo studies have established that pituitary nitric oxide synthase type 1 (NOS1) is regulated by gonadotropin-releasing hormone (GnRH). The aim of our study was to elucidate the mechanisms of NOS1 regulation by GnRH in rat pituitary cells. Using a perifused cell system, we demonstrated that NOS1 induction was sensitive to GnRH pulse frequency and was maximally induced under continuous GnRH stimulation. In primary cultures of rat pituitary cells, sustained stimulation with the GnRH agonist triptorelin (GnRHa) increased NOS1 protein levels, whereas NOS2 and NOS3 levels were unaffected. NOS1 up-regulation occurred in gonadotroph cells only, in a time-dependent and concentration-dependent manner (maximum increase, 2.5-fold; half-maximal concentration, 0.17 nM). GnRHa effect was mimicked by cAMP pathway activators and, most importantly, was blocked by disruption of the protein kinase A (PKA) pathway using pharmacological inhibitors such as Rp-cAMP or drug phosphatase technology-protein kinase inhibitor (DPT-PKI), a cell-permeant PKI peptide. In contrast, modulation of the PKC pathway and inhibition of the MAPK cascade were ineffective. Overall, these experiments demonstrated that GnRH-induced up-regulation of pituitary NOS1 is mediated notably by the cAMP/PKA pathway. Last, in vivo administration of a GnRH antagonist markedly inhibited the pituitary cAMP rise at proestrus in addition to suppressing NOS1 increase. Altogether, our data suggest that the cAMP/PKA signaling pathway is preferentially recruited under sustained GnRH stimulation in vivo during proestrus, allowing the expression of a specific set of PKA-regulated proteins, including NOS1, in gonadotroph cells.

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Section: Discussionmentioning

confidence: 99%

Sustained Gonadotropin-Releasing Hormone Stimulation Mobilizes the cAMP/PKA Pathway to Induce Nitric Oxide Synthase Type 1 Expression in Rat Pituitary Cells In Vitro and In Vivo at Proestrus1

Garrel

Simon

Thieulant

et al. 2010

Biology of Reproduction

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“…FS cells have been shown to produce a range of growth factors and cytokines, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor, annexin 1 (ANXA1) and interleukin-6, as well as nitric oxide (NO), 4 all of which have clear roles in the regulation of specific endocrine pituitary cell types. For example, in the embryo, NO has been shown to increase both growth hormone gene expression and the number of somatotrophs, 33 whereas FS cell (intriguingly those near blood vessels) NO synthase expression has been shown to be increased by dopamine, potentially mediating some of the inhibitory actions of this small transmitter on prolactin release. 34 To this list, we can now add the Wnt ligands because these have been shown to be secreted from Sox2-positive stem cells.…”

Section: Communication With Other Pituitary Cell Typesmentioning

confidence: 99%

Renewing an old interest: Pituitary folliculostellate cells

Tissier

Mollard

2021

J Neuroendocrinology

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Increasingly, neuroendocrine research focuses on its potential for an impact of novel findings on highly-prevalent human health problems, in particular those where the underlying physiology and its dysfunction is poorly understood. Research on the pituitary, the master gland relaying hormonal information between the brain and many peripheral tissues, cannot escape this trend, as exemplified by the growing hope of regenerative medicine with the recent discovery of adult stem cells in the pituitary parenchyma. One exciting aspect of stem cell therapy is its potential to correct a number of pituitary disorders with aetiologies that are poorly understood. This focus on stem cells and their potential may explain how a subpopulation of pituitary cells, devoid of secretory granules, has changed from being described as folliculostellate (FS) cells (coined by Evelyne Vila-Porcile in 1972 1 ) to adult Sox2+ve stem cells. Recent studies have highlighted an important aspect of these stem cells, in that they are the

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“…NO can act both intracellularly as a second messenger and extracellularly as a conveyor of information between cells [9] and it also acts as a neuromodulator in the endocrine system [10], including the somatotrophic axis [11]. Recently, an increasing body of evidence confirms that NO is involved in the regulation of GH secretion both in somatotrophs [12,13] and GH-releasing adenomas [14,15]. Simultaneously, NO may restrain rather than mediate the apoptotic effect of tumor necrosis factor (TNF)-alpha in rat anterior pituitary cells [16].…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells

Tian

Wang

et al. 2010

Endocr

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Ghrelin stimulates growth hormone release and cell proliferation, which strongly supports a significant role for this peptide in the control of growth hormone-releasing adenomas function and growth. Nitric oxide can influence the stimulatory effects of ghrelin on growth hormone secretion in growth hormone-releasing adenomas. However, the effect of nitric oxide (NO) on ghrelin-induced cell proliferation and the mechanism of this effect in the adenoma were not clarified. In this study, we observed that ghrelin, at a concentration of 10⁻⁹ to 10⁻⁶ M, significantly increased BrdU incorporation into rat GH3 cells. A NO donor, S-nitroso-N-acetylpenicillamine (SNAP), blunted basal, and ghrelin-induced cell proliferation. A blocker of NO synthase, Nw-nitro-L-arginine methyl ester hydrochloride (NAME), had no influence on these actions. The activation of extracellular signal-regulated kinase (ERK) 1/2 was examined by western blotting. The results showed that SNAP reduced ghrelin-stimulated ERK1/2 activation but NAME had no influence on this activation. Together, this study indicates that NO inhibited ghrelin-induced cell proliferation by blocking ERK1/2 activation in GH3 cells.

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Nitric oxide stimulates embryonic somatotroph differentiation and growth hormone mRNA and protein expression through a cyclic guanosine monophosphate-independent mechanism

Cited by 3 publications

References 40 publications

Sustained Gonadotropin-Releasing Hormone Stimulation Mobilizes the cAMP/PKA Pathway to Induce Nitric Oxide Synthase Type 1 Expression in Rat Pituitary Cells In Vitro and In Vivo at Proestrus1

Sustained Gonadotropin-Releasing Hormone Stimulation Mobilizes the cAMP/PKA Pathway to Induce Nitric Oxide Synthase Type 1 Expression in Rat Pituitary Cells In Vitro and In Vivo at Proestrus1

Renewing an old interest: Pituitary folliculostellate cells

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells

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