Molecular mechanisms involved in LH release by the ovine pituitary cells

Yang, Dominique; Caraty, Alain; Dupont, Joëlle

doi:10.1016/j.domaniend.2005.02.015

Cited by 13 publications

(6 citation statements)

References 54 publications

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“…In pituitary cell cultures, IGF-1 has been demonstrated to increase the release of gonadotrophin via the IGF-1R (Kanematsu et al 1991), enhancing the secretory response to gonadotrophin-releasing hormone (Soldani et al 1994;Yang et al 2005). In agreement with these reports, we have observed that IGF-1-stimulated gonadotroph cells exhibit the fine-structural features of high biosynthetic activity.…”

Section: Discussionsupporting

confidence: 90%

Ultrastructural immunolocalization of IGF-1 and insulin receptors in rat pituitary culture: evidence of a functional interaction between gonadotroph and lactotroph cells

et al. 2006

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We have investigated the expression of receptors for insulin and insulin-like growth factor 1 (IGF-1) in rat pituitary cells in vitro and examined the morphological and proliferative changes induced in adenohypophyseal cells by insulin and IGF-1. The proliferation of lactotrophs was determined by double-immunostaining for bromodeoxyuridine and prolactin. Incubation with insulin (10, 100 or 1000 ng/ml) or IGF-1 (5, 30 or 100 ng/ml) for 48 or 72 h significantly increased the number of lactotrophs undergoing mitosis. Co-incubation of insulin or IGF-1 with genistein (25 microM), an inhibitor of the tyrosine kinase receptor, reduced the proliferation of lactotrophs elicited by the hormone and the growth factor. The receptors for insulin and IGF-1 were localized in intact pituitary cells by ultrastructural immunocytochemistry with the colloidal gold-protein A technique. Gonadotrophs expressed both receptors, specific labelling being restricted to this cell type. Electron-microscopical observations of pituitary cell cultures incubated with insulin or IGF-1 revealed gonadotroph cells exhibiting the fine-structural features of enhanced protein synthetic activity. These findings suggest that both insulin and IGF-1 are able to induce the proliferation of lactotrophs through an indirect mechanism mediated by a factor synthesized by gonadotroph cells, in addition to stimulating the biosynthetic activity of the gonadotroph in a direct manner.

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Section: Discussionsupporting

confidence: 90%

Ultrastructural immunolocalization of IGF-1 and insulin receptors in rat pituitary culture: evidence of a functional interaction between gonadotroph and lactotroph cells

et al. 2006

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“…2), and as previously shown in the white adipose tissue (Zhang et al 2005), maintains the activation of MAPK by protecting it from the effects of a MAPK-specific phosphatase (Kim et al 2001, Navratil et al 2010. The signal pathways activated by GnRH-R include major members of the MAPK family (Yang et al 2005, Dobkin-Bekman et al 2006. Opn3 has been shown to be involved in light sensation and circadian rhythms, with its implicated function being light reception for light-induced exocytosis in the PC12 cells and primary embryonic telencephalon cells (Henkel et al 2006).…”

Section: Cmentioning

confidence: 86%

Identification of estradiol/ERα-regulated genes in the mouse pituitary

Kim¹,

Gieske²,

Trudgen³

et al. 2011

Journal of Endocrinology

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Estrogen acts to prime the pituitary prior to the GnRHinduced LH surge by undiscovered mechanisms. This study aimed to identify the key components that mediate estrogen action in priming the pituitary. RNA extracted from the pituitaries of metestrous (low estrogen) and proestrus (high estrogen) stage mice, as well as from ovariectomized wildtype and estrogen receptor a (ERa) knockout mice treated with 17b-estradiol (E 2 ) or vehicle, was used for gene expression microarray. Microarray data were then aggregated, built into a functional electronic database, and used for further characterization of E 2 /ERa-regulated genes. These data were used to compile a list of genes representing diverse biological pathways that are regulated by E 2 via an ERa-mediated pathway in the pituitary. This approach substantiates ERa regulation of membrane potential regulators and intracellular vesicle transporters, among others, but not the basic components of secretory machinery. Subsequent characterization of six selected genes (Cacna1a, Cacna1g, Cited1, Abep1, Opn3, and Kcne2) confirmed not only ERa dependency for their pituitary expression but also the significance of their expression in regulating GnRH-induced LH secretion. In conclusion, findings from this study suggest that estrogen primes the pituitary via ERa by equipping pituitary cells with critical cellular components that potentiate LH release on subsequent GnRH stimulations.

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“…On the other hand, FSH secretion is not as rigidly linked to pulsatile input of GnRH (34,35), and passive secretion may occur. Because GnRH activates ERK and other second messengers (36,37), we have examined E17␤ action in relation to this. Phosphorylated second messenger levels would be expected to vary over time in relation to GnRH stimulus in the control (vehicle-treated) OVX-HPD animals.…”

Section: Discussionmentioning

confidence: 99%

Rapid in Vivo Effects of Estradiol-17β in Ovine Pituitary Gonadotropes Are Displayed by Phosphorylation of Extracellularly Regulated Kinase, Serine/Threonine Kinase, and 3′,5′-Cyclic Adenosine 5′-Monophosphate-Responsive Element-Binding Protein

2007

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We have determined the time course of phosphorylation of MAPK/ERK, cAMP-responsive element-binding protein (CREB), and serine/threonine kinase (Akt) in ovine pituitary gonadotropes after in vivo injection (iv) of either 25 mug estradiol-17beta (E17beta) or vehicle. In ovariectomized ewes, E17beta increased the number of gonadotropes expressing phosphorylated (p)ERK-1/2 and pCREB immunoreactivity (-IR) within 90 min, as assessed by immunohistochemistry. By Western blot, we also showed that pERK-1/2, pCREB, and pAkt (ser 473) proteins were up-regulated by E17beta. In ovariectomized, hypothalamo-pituitary-disconnected animals, gonadotrope function was restored with hourly GnRH pulses (iv), and E17beta injection (iv) reduced LH response within 1 h. Immunohistochemistry showed that E17beta increased pERK-1/2-IR in gonadotropes within 15 min and peak response at 60 min. The number of cells immunoreactive for pCREB was greater in E17beta-treated animals than in vehicle-injected controls at 60 and 90 min. Western blot revealed a pERK-1/2 response within 15 min and pCREB response at 30 min. Up-regulation of pAkt occurred within 60 min of E17beta treatment. Thus, rapid effects of E17beta on gonadotropes involve phosphorylation of second messenger proteins with a time course that may relate to the rapid negative feedback effect to reduce responsiveness to GnRH.

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Molecular mechanisms involved in LH release by the ovine pituitary cells

Cited by 13 publications

References 54 publications

Ultrastructural immunolocalization of IGF-1 and insulin receptors in rat pituitary culture: evidence of a functional interaction between gonadotroph and lactotroph cells

Ultrastructural immunolocalization of IGF-1 and insulin receptors in rat pituitary culture: evidence of a functional interaction between gonadotroph and lactotroph cells

Identification of estradiol/ERα-regulated genes in the mouse pituitary

Rapid in Vivo Effects of Estradiol-17β in Ovine Pituitary Gonadotropes Are Displayed by Phosphorylation of Extracellularly Regulated Kinase, Serine/Threonine Kinase, and 3′,5′-Cyclic Adenosine 5′-Monophosphate-Responsive Element-Binding Protein

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