Gonadotropin-Releasing Hormone-Stimulated Phosphoinositide Hydrolysis in the Anterior Pituitary

Sortino, Maria Angela; Evans, William S.; Speciale, C.; Thorner, Michael O.; Scapagnini, U.; MacLeod, Robert M.; Canonico, Pier Luigi

doi:10.1159/000125061

Cited by 14 publications

(4 citation statements)

References 14 publications

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“…The suppressive effect of PLC, but not of PMA, on GnRH-stimulated LH glycosylation may be related to the low dose of PMA (10 nM) used in this study. This interpretation is consistent with the observa tion that the GnRH-stimulated pituitary inositol phos phate accumulation can be attenuated by PMA at doses equal to or greater than 30 nM [43,44], Alternatively, it may be attributed to signals generated by PLC which affect compounds other than PKC. These may include products of polyphospholipid metabolism other than dia- 66 Liu/Pu/Jackson PLC in LH Biosynthesis and Release cyigiycerol, or some undefined factors involved in the nonspecific action of PLC.…”

Section: Discussionsupporting

confidence: 90%

Differential Actions of Phospholipase C on Gonadotropin Releasing-Hormone-Stimulated Release and Glycosylation of Luteinizing Hormone in Rat Anterior Pituitary Cells

Liu¹,

Pu²,

Jackson

1994

Neuroendocrinology

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Receptor-mediated activation of phospholipase C (PLC) which releases diacylglycerol and inositol trisphosphate has been implicated in the action of gonadotropin-releasing hormone (GnRH) on gonadotrophs. Previously we demonstrated that the synthetic diacylglycerol, phorbol 12-myristate 13-acetate (PMA) and PLC mimic the stimulatory effects of GnRH on both luteinizing hormone (LH) glycosylation and release. In this study we further investigated how PMA or PLC interact with GnRH to control LH release versus glycosylation. Cultured pituitary cells were incubated in the presence of radio-labeled precursors and GnRH (0, 1, or 100 nM), with or without PMA (10 nM) or PLC (0.24 U/ml) for 4 h. LH translation and glycosylation were monitored by measuring incorporation of [¹⁴C]alanine and [³H]glucosamine, respectively, into total (cell and medium) immunoprecipitable LH. Immunoreactive LH (IRLH) was measured by radioimmunoassay. Both PMA and PLC increased (p < 0.01) basal IRLH release, and IRLH release stimulated by 1 nM GnRH. Neither PMA nor PLC exerted an additive effect on IRLH release stimulated by 100 nM GnRH. The interactions between PMA or PLC and GnRH on IRLH release were significant (p < 0.01). Both PMA and PLC elevated (p < 0.01) total [³H]glucosamine-LH, but had no additive effect with 1 nM GnRH; PLC depressed (p < 0.05) the stimulatory effect of 100 nM GnRH, whereas PMA had no effect. The interactions between PMA or PLC and GnRH on LH glycosylation were significant (p < 0.01). PMA, PLC or GnRH alone did not affect total [¹⁴C]alanine-LH. In the presence of 1 or 100 nM GnRH, PLC, but not PMA, decreased (p < 0.05) total [¹⁴C]alanine-LH. However, there was no significant interaction between PLC and GnRH on LH translation. In summary, PMA, PLC or GnRH alone stimulated LH release and glycosylation. PLC and GnRH interacted to modulate LH release and LH glycosylation in a different manner, whereas PMA and GnRH interacted to modulate these two parameters similarly. PLC may be involved in the negative feedback regulation of LH glycosylation, but not of LH release.

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Section: Discussionsupporting

confidence: 90%

Differential Actions of Phospholipase C on Gonadotropin Releasing-Hormone-Stimulated Release and Glycosylation of Luteinizing Hormone in Rat Anterior Pituitary Cells

Liu¹,

Pu²,

Jackson

1994

Neuroendocrinology

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“…The ER, with its Ca 2 +-binding proteins, is an intracellular Ca2+-store (Macer and Koch 1988). Release of Ca 2 + from this intracellular source is mediated by IP3, a second messenger which is formed after binding of G n R H to its receptor (Guillemette et al 1987;Sortino et al 1988). It appears that in several investigated cell types only certain compartments of the ER release Ca 2 + in respons to IP3, in fact there are IPa-sensitive and IP3-insensitive Ca2+-pools (Jean and Klee 1986;Nicchitta et al 1987;Leslie et al 1988 ;Dawson and Comerford 1989;Schulz et al 1989).…”

Section: Discussionmentioning

confidence: 99%

“…For teleost species scarce information is Offprint requests to: J. Peute available about post-receptor systems in GTH-cells. In mammals it was shown that inositol 1,4,5-triphosphate (IP3) and diacylglycerol are important second messengers (Berridge 1984;Hirota et al 1985;Sortino et al 1988;Clayton 1989). Likewise, Ca 2+ is a necessary factor in the regulation of GTH release, as was illustrated by the rise in intracellular Ca2+-concentration after binding of G n R H to its receptor, whereas absence of Ca 2+ or blocking the Ca/+-infiux attenuates GTH-secretion in response to GnRH (Conn 1982;Bates and Conn 1984;Chang et al 1988;Drouva et al 1988).…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural localization of calcium and Ca2+-ATPase activity in gonadotrops and stellate cells of the catfish pituitary

Peute¹,

Linder²,

Zandbergen³

et al. 1990

Histochemistry

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In the pituitary of the African catfish, Clarias gariepinus, calcium precipitates were ultrastructurally visualized with the oxalate-pyroantimonate procedure (OPP). The presence of calcium in these precipitates was validated with several methods, including "Electron Energy Loss Spectrometry" (EELS). In the OPP-treated tissue calcium precipitates were seen in a) non-secretory stellate cells and b) gonadotropic (GTH-) cells. In the latter the amount of precipitate is generally low, but stimulation of the gonadotropin release, either in vivo or in vitro, resulted in a considerable increase. This increase is discussed in relation to the role of calcium as second messenger in the GTH-cells. Ca(2+)-ATPase was exclusively represented in stellate cells and GTH-cells, its strongest activity associated with the plasma membrane and with the membranes of the endoplasmic reticulum. The localization of this enzyme is discussed in relation to its role in the regulation of the intracellular calcium concentration in the GTH-cells. The stellate cells are considered to be involved in the regulation of extracellular calcium concentrations in the pituitary.

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“…In gonadotropes, GnRH acts on protein kinase C and mobilizes calcium-calmodulin [74][75][76][77]. GnRH also acts on cell membranes by enhancing calcium entry through L-and N-type calcium channels in female [72] but not male [78] gonadotropes, whereas GnRH blocks N-type calcium currents in bullfrog sympathetic ganglia [72].…”

Section: Animal Studies Of Gnrh Analogsmentioning

confidence: 99%

Relationship of Reproductive Hormones and Neuromuscular Disease of the Gastrointestinal Tract

Mathias¹,

Clench²

1998

Dig Dis

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Functional disorders of the gastrointestinal tract comprise a common but ill-defined group of diseases; they primarily afflict women. Although predominantly involving nerve and muscle, the cellular and molecular bases of the pathogenesis of these functional disorders are unknown. Clinical studies indicate that some result from neural dysfunction within the enteric nervous system, others may be due to muscular problems, and the causes of still others remain unknown. Laboratory studies have shown that ovarian products such as progesterone, luteinizing hormone, human chorionic gonadotropin, and relaxin (but not estrogen), are neural antagonists of gastrointestinal motility. The production and secretion of these ovarian substances are controlled by gonadotropin-releasing hormone (GnRH) released from the hypothalamus; they probably act on γ-aminobutyric acid receptors and alter chloride influx into the cell. GnRH analogs are effective drugs that downmodulate the hypothalamic-pituitary-gonadal axis and inhibit the secretion of gonadal products involved in such hormone-dependent diseases as endometriosis and prostate cancer. Acting on the GnRH receptors (seven transmembrane domain receptors) on myenteric neurons, GnRH analogs are also effective neural modulators in such disorders as functional bowel disease. These analogs are a promising new group of compounds that may be used to treat difficult gastrointestinal problems.

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Gonadotropin-Releasing Hormone-Stimulated Phosphoinositide Hydrolysis in the Anterior Pituitary

Cited by 14 publications

References 14 publications

Differential Actions of Phospholipase C on Gonadotropin Releasing-Hormone-Stimulated Release and Glycosylation of Luteinizing Hormone in Rat Anterior Pituitary Cells

Differential Actions of Phospholipase C on Gonadotropin Releasing-Hormone-Stimulated Release and Glycosylation of Luteinizing Hormone in Rat Anterior Pituitary Cells

Ultrastructural localization of calcium and Ca2+-ATPase activity in gonadotrops and stellate cells of the catfish pituitary

Relationship of Reproductive Hormones and Neuromuscular Disease of the Gastrointestinal Tract

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