Relevant bibliographies by topics / Gonadotrophin Hormone Releasing Hormone (GnRH)

Academic literature on the topic 'Gonadotrophin Hormone Releasing Hormone (GnRH)'

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Published: 10 December 2022
Last updated: 19 February 2023

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Journal articles on the topic "Gonadotrophin Hormone Releasing Hormone (GnRH)"

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Leaños-Miranda, Alfredo, Alfredo Ulloa-Aguirre, Laura A. Cervini, Jo Ann Janovick, Jean Rivier, and P. Michael Conn. "Identification of new gonadotrophin-releasing hormone partial agonists." Journal of Endocrinology 189, no. 3 (June 2006): 509–17. http://dx.doi.org/10.1677/joe.1.06724.

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GnRH agonists or antagonists are currently utilized as therapeutic agents in a number of diseases. A side-effect of prolonged treatment with GnRH analogues is hypoestrogenism. In this study, we tested the in vitro potency of different GnRH analogues originally found to be partial agonists (i.e. analogues with decreased efficacy for activating or stimulating their cognate receptor) as well as novel analogues, to identify compounds that might potentially be useful for partial blockade of gonadotrophin release. Cultured COS-7 cells transiently expressing the rat or human GnRH receptor (GnRHR) were exposed to increasing concentrations (10−8 to 10−5 M) of GnRH analogues (c(4–10)[Asp4,DNal6,Dpr10]-GnRH; c(4–10) [Dpr4,DNal6,Asp10]-GnRH; c(4–10)[Cys4,10,DNal6]-GnRH; c[Eaca1,DNal6]-GnRH; c[Gly1,DNal6]-GnRH; c[βAla1,DTrp6]-GnRH; c[Dava1,DNal6]-GnRH; c[Gaba1, DNal6]-GnRH), and the ability of these analogues to provoke or antagonize GnRH-stimulated inositol phosphate production was assessed. With both human and rat GnRHRs, c[Eaca1,DNal6]-GnRH, c[Gly1,DNal6]-GnRH, c[βAla1,DTrp6]-GnRH and c[Dava1,DNal6]-GnRH exhibited partial agonist activity (35–87% of the maximal efficacy shown by 10−6 M GnRH), whereas c[Gaba1,DNal6]-GnRH behaved as a partial agonist with the human GnRHR and as full agonist with the rat GnRHR. c(4–10)[Asp4, DNal6,Dpr10]-GnRH and c(4–10)[Dpr4,DNal6,Asp10]-GnRH exhibited full antagonist activity with both GnRHRs, and c(4–10) [Cys4,10,DNal6]-GnRH was a weak, partial agonist with the human GnRHR and a full antagonist with the rat GnRHR. With the exception of c[Gaba1,DNal6]-GnRH stimulation of the human GnRHR, and c[Dava1,DNal6]-GnRH and c[Gaba1, DNal6]-GnRH stimulation of the rat GnRHR, all partial agonists also exhibited antagonist activity in the presence of the exogenous full agonist. The results demonstrate that structurally similar analogues display variable potencies and efficacies in vitro for a specific GnRHR as well as for the human versus the rat GnRHR. Their ultimate in vivo usefulness to treat clinical conditions in which complete suppression of gonadotroph activity is not required remains to be investigated.
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2

King, J. A., J. S. Davidson, and R. P. Millar. "Interaction of endogenous chicken gonadotrophin-releasing hormone-I and -II on chicken pituitary cells." Journal of Endocrinology 117, no. 1 (April 1988): 43–49. http://dx.doi.org/10.1677/joe.0.1170043.

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ABSTRACT The presence of two endogenous forms of gonadotrophin-releasing hormone (GnRH) in the chicken hypothalamus (chicken GnRH-I ([Gln8]GnRH) and chicken GnRH-II ([His5,Trp7,Tyr8]GnRH)), and the stimulation of gonadotrophins by both forms, suggests the possible existence of GnRH receptor subtypes and gonadotroph subtypes in the chicken pituitary. This question was investigated by assessing the effects of various combinations of the two known forms of chicken hypothalamic GnRH and antagonist analogues of GnRH on LH release from dispersed chicken anterior pituitary cells in both static and perifused systems. The relative inhibition of chicken GnRH-I-stimulated and chicken GnRH-II-stimulated LH release by 12 GnRH antagonists did not differ significantly, suggesting a single GnRH receptor type. Chicken GnRH-II was approximately sixfold more potent than chicken GnRH-I in releasing LH. Release of LH in response to maximal doses of chicken GnRH-I and chicken GnRH-II and to a mixture of both was similar and the two peptides were not additive in their effects, consistent with the presence of a single type of LH gonadotroph and a GnRH receptor which binds both forms of GnRH. Each form of GnRH desensitized cells to subsequent stimulation with the other form, providing additional evidence for a single type of LH gonadotroph. These findings suggest that chicken GnRH-I and -II stimulate gonadotrophin release through a single GnRH receptor type on a single class of LH gonadotroph in the chicken pituitary. J. Endocr. (1988) 117,43–49
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Wilson, C. A., A. J. Leigh, and A. J. Chapman. "Gonadotrophin glycosylation and function." Journal of Endocrinology 125, no. 1 (April 1990): 3–14. http://dx.doi.org/10.1677/joe.0.1250003.

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ABSTRACT This review emphasizes the heterogeneous structure of the gonadotrophin hormones and the influence of different oligosaccharide structures on the bioactivity of these hormones. A summary has been made of the changes in biopotency of the gonadotrophins throughout the life-cycle of the human and in different endocrine states in the rat. In general it appears that the charge of the gonadotrophin conferred by the acid radicals attached to the terminal groups on the oligosaccharide structures strongly influences biopotency. Basic structures have a greater potency in in-vitro assays, but a short half-life in the circulation, while acidic isoforms are less potent, but have a longer circulatory time and are thus more active in in-vivo estimations. More basic forms are secreted over the adult reproductive years compared with the prepubertal period and old age. The glycosyl structure of the carbohydrate groups also alters in different endocrine states and is probably also important for the bioactivity and potency of the hormone. Gonadotrophin-releasing hormone (GnRH) and gonadal steroids can influence the type of isoform synthesized and released, and therefore affect the function of gonadotrophins. GnRH enhances glycosylation, sulphation and biopotency. Oestradiol potentiates the glycosylation induced by GnRH and reduces sialylation, while testosterone increases sialylation. Journal of Endocrinology (1990) 125, 3–14
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Goto, K., F. Kotsuji, and T. Tominaga. "Divergent effects of gonadotrophin-releasing hormone (GnRH) analogue and authentic GnRH on the anterior pituitary gland of rats with restricted feeding." Journal of Endocrinology 145, no. 3 (June 1995): 501–11. http://dx.doi.org/10.1677/joe.0.1450501.

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Abstract The effects of gonadotrophin-releasing hormone analogue (GnRHa; buserelin) on the pituitary function and morphology of food-restricted rats were compared with those of authentic GnRH. After adult female rats had been restricted to 10 g food/day for 60 days, various doses of GnRHa (10 ng, 100 ng and 1 μg) or GnRH (10 μg) were administered either daily for 7 days or twice a week for 4 weeks from day 61 of the period of underfeeding. Underfeeding brought about a decrease in the pituitary gonadotrophin content, serum levels of gonadotrophins and oestradiol, and the number and size of both LH- and FSH-positive pituitary cells. Daily and/or twice-weekly administration of authentic GnRH to underfed rats produced an increase in pituitary and serum gonadotrophin levels and the number and size of both LH- and FSH-positive pituitary cells. The administration of GnRHa daily for 7 days increased serum gonadotrophin levels, while it produced a reduction in the pituitary gonadotrophin content and number and size of both LH- and FSH-positive pituitary cells in a dose-dependent manner. Twice-weekly administration of GnRHa also produced an elevation of serum gonadotrophin levels and reduction of pituitary gonadotrophin content, although it did not affect the numbers and areas of LH- and FSH-positive pituitary cells. A GnRH loading test performed after the GnRHa treatment showed that the GnRHa treatment performed in this study did not produce down-regulation of the GnRH receptor. Thus, it can be concluded that the gonadotrophin-synthesizing activity of GnRHa is weaker than that of authentic GnRH, or that GnRHa may preferentially exert gonadotrophin-releasing activity rather than gonadotrophin-synthesizing activity in the anterior pituitary of underfed rats. Journal of Endocrinology (1995) 145, 501–511
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Bosma, P. T., S. M. Kolk, F. E. M. Rebers, O. Lescroart, I. Roelants, P. H. G. M. Willems, and R. W. Schulz. "Gonadotrophs but not somatotrophs carry gonadotrophin-releasing hormone receptors: receptor localisation, intracellular calcium, and gonadotrophin and GH release." Journal of Endocrinology 152, no. 3 (March 1997): 437–46. http://dx.doi.org/10.1677/joe.0.1520437.

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Gonadotrophs are the primary target cells for GnRH in the pituitary. However, during a limited period of neonatal life in the rat, lactotrophs and somatotrophs respond to GnRH as well. Also, in the adults of a number of teleost fishes (e.g. carp, goldfish, and tilapia but not trout), GnRH is a potent GH secretagogue. In studying hypophysiotrophic actions of the two forms of GnRH present in the African catfish (Clarias gariepinus), chicken GnRH-II ([His5,Trp7,Tyr8]GnRH; cGnRH-II) and catfish GnRH ([His5,Asn8]GnRH; cfGnRH), we have investigated the effects of GnRH on catfish gonadotrophs and somatotrophs. GnRH binding was examined by incubating dispersed pituitary cells attached to coverslips with 125I-labelled [d-Arg6,Trp7,Leu8,Pro9-Net]GnRH (sGnRHa), a salmon GnRH analogue with high affinity for the GnRH receptor. Following fixation and immunohistochemistry using antisera against catfish LH and GH, 125I-labelled sGnRHa was localised autoradiographically and silver grains were quantified on gonadotrophs and somatotrophs. Specific binding of 125I-labelled sGnRHa was restricted to gonadotrophs. Both cfGnRH and cGnRH-II dose-dependently inhibited 125I-labelled sGnRHa binding to gonadotrophs. To substantiate the localisation of functional GnRH receptors, the effects of cfGnRH and cGnRH-II on the cytosolic free calcium concentration ([Ca2+]i) were examined in Fura-2-loaded somatotrophs and gonadotrophs. GnRH-induced increases in [Ca2+]i appeared to be confined to gonadotrophs, in which both endogenous GnRHs caused a single and transient increase in [Ca2+]i. The amplitude of this [Ca2+]i transient depended on the GnRH dose and correlated well with the GnRHs' effect on LH release. In vivo experiments demonstrated that GnRH treatments which markedly elevated plasma LH levels had no effect on plasma GH levels, while a dopamine agonist (apomorphine) significantly elevated plasma GH levels. We conclude that the two endogenous forms of GnRH in the African catfish are not directly involved in the regulation of the release of GH, suggesting that GnRHs cannot be considered as GH secretagogues in teleosts in general. Journal of Endocrinology (1997) 152, 437–446
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Evans, J. J., G. Robinson, and K. J. Catt. "Gonadotrophin-releasing activity of neurohypophysial hormones: I. Potential for modulation of pituitary hormone secretion in rats." Journal of Endocrinology 122, no. 1 (July 1989): 99–106. http://dx.doi.org/10.1677/joe.0.1220099.

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ABSTRACT Neurohypophysial hormones have been implicated in the control of anterior pituitary function, and oxytocin has been shown to stimulate gonadotrophin excretion and ovarian follicular development in certain species. To determine the role of neurohypophysial peptides in the control of gonadotrophin release, their actions on LH and FSH secretion were analysed in rats in vivo and in vitro. In adult female rats, administration of oxytocin during early pro-oestrus advanced the spontaneous LH surge and markedly increased peripheral LH levels at 15.00 h compared with control animals. In cultured pituitary cells from adult female rats, oxytocin and vasopressin elicited dose-related increases in LH and FSH release. Such responses were not affected by a potent gonadotrophin-releasing hormone (GnRH) antagonist that abolished GnRH agonist-induced release of LH and FSH. Oxytocin did not enhance GnRH agonist-stimulated gonadotrophin release to the same extent as it increased basal secretion, but at low concentrations of GnRH agonist the effects were additive. The gonadotrophin responses to oxytocin and vasopressin were inhibited by the specific neurohypophysial hormone antagonists, [d(CH2)5d-Ile2,Ile4,Arg8]vasopressin and [d(CH2)5Tyr (Me),Arg8]vasopressin. These results provide direct evidence that neurohypophysial hormones can stimulate gonadotrophin secretion through a receptor system distinct from the GnRH receptor. Such a mechanism could represent a complementary hypothalamic control system for long-term modulation of LH and FSH secretion by exerting a basal or tonic influence on gonadotrophin production. Journal of Endocrinology (1989) 122, 99–106
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Bonnin, M., M. Mondain-Monval, M. C. Audy, and R. Scholler. "Basal and gonadotropin releasing hormone stimulated gonadotropin levels in the female red fox (Vulpes vulpes L.). Negative feedback of ovarian hormones during anoestrus." Canadian Journal of Zoology 67, no. 3 (March 1, 1989): 759–65. http://dx.doi.org/10.1139/z89-107.

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In the red fox, Vulpes vulpes L., an inhibition of gonadotropic function is observed in early anoestrus, particularly during lactation. During this period, secretion of progesterone as a result of the persistent corpora lutea after parturition and episodic releases of estradiol signify ovarian activity, suggesting involvement of these hormones in the modulation of pituitary hormones (luteinizing hormone (LH), follicle-stimulating hormone (FSH)). Effects of ovariectomy and (or) progesterone or estradiol treatments in vivo upon basal and gonadotropin releasing hormone (GnRH)-stimulated LH and FSH were observed. After ovariectomy, a great increase in the basal level of both gonadotropins and in GnRH-stimulated LH release, but not GnRH-stimulated FSH release, were observed. Progesterone treatment induced a decrease in GnRH-stimulated LH and FSH secretions and a decrease in basal LH and FSH levels in ovariectomized females. Estradiol treatment abolished basal secretions and GnRH responses for both hormones. These results suggest a negative feedback of both ovarian steroids at the hypothalamopituitary level on LH and FSH secretions during early anoestrus.
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Kotsuji, F., K. Hosokawa, and T. Tominaga. "Effects of the daily administration of gonadotrophin-releasing hormone on the anterior pituitary gland of rats with restricted feeding." Journal of Endocrinology 134, no. 2 (August 1992): 177—NP. http://dx.doi.org/10.1677/joe.0.1340177.

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ABSTRACT To investigate the influence of weight reduction on pituitary function and its modulation by gonadotrophin-releasing hormone (GnRH), female rats were restricted to 10 g food/day for 60 days. GnRH (5 μg) or saline (0·2 ml) were administered daily between days 31 and 60 of the period of underfeeding. Underfeeding brought about a decrease in the pituitary gonadotrophin content, serum levels of gonadotrophins and oestradiol, and the number and size of both LH- and FSH-positive pituitary cells. The administration of GnRH to underfed rats produced an increase in the pituitary and serum gonadotrophin levels and the number and size of both LH- and FSH-positive pituitary cells. These observations suggest that underfeeding and/or weight loss diminish the number and activity of the pituitary gonadotrophs, and that daily administration of GnRH both increases the number of gonadotrophs and augments their activity. Journal of Endocrinology (1992) 134, 177–182
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Moncaut, Natalia, Gustavo Somoza, Deborah M. Power, and Adelino V. M. Canário. "Five gonadotrophin-releasing hormone receptors in a teleost fish: isolation, tissue distribution and phylogenetic relationships." Journal of Molecular Endocrinology 34, no. 3 (June 2005): 767–79. http://dx.doi.org/10.1677/jme.1.01757.

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Gonadotrophin-releasing hormone (GnRH) is the main neurohormone controlling gonadotrophin release in all vertebrates, and in teleost fish also of growth hormone and possibly of other adenohypophyseal hormones. Over 20 GnRHs have been identified in vertebrates and protochoordates and shown to bind cognate G-protein couple receptors (GnRHR). We have searched the puffer fish, Fugu rubripes, genome sequencing database, identified five GnRHR genes and proceeded to isolate the corresponding complementary DNAs in European sea bass, Dicentrachus labrax. Phylogenetic analysis clusters the European sea bass, puffer fish and all other vertebrate receptors into two main lineages corresponding to the mammalian type I and II receptors. The fish receptors could be subdivided in two GnRHR1 (A and B) and three GnRHR2 (A, B and C) subtypes. Amino acid sequence identity within receptor subtypes varies between 70 and 90% but only 50–55% among the two main lineages in fish. All European sea bass receptor mRNAs are expressed in the anterior and mid brain, and all but one are expressed in the pituitary gland. There is differential expression of the receptors in peripheral tissues related to reproduction (gonads), chemical senses (eye and olfactory epithelium) and osmoregulation (kidney and gill). This is the first report showing five GnRH receptors in a vertebrate species and the gene expression patterns support the concept that GnRH and GnRHRs play highly diverse functional roles in the regulation of cellular functions, besides the “classical” role of pituitary function regulation.
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Lajkó, Eszter, Éva Pállinger, Zsombor Kovács, Ildikó Szabó, and László Kőhidai. "Effects of Gonadotropin-Releasing Hormone (GnRH) and Its Analogues on the Physiological Behaviors and Hormone Content of Tetrahymena pyriformis." International Journal of Molecular Sciences 20, no. 22 (November 14, 2019): 5711. http://dx.doi.org/10.3390/ijms20225711.

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The unicellular Tetrahymena distinguishes structure-related vertebrate hormones by its chemosensory reactions. In the present work, the selectivity of hormone receptors was evaluated by analyzing the effects of various gonadotropin-releasing hormone (GnRH) analogs (GnRH-I, GnRH-III) as well as truncated (Ac-SHDWKPG-NH2) and dimer derivatives ([GnRH-III(C)]2 and [GnRH-III(CGFLG)]2) of GnRH-III on (i) locomotory behaviors, (ii) cell proliferation, and (iii) intracellular hormone contents of Tetrahymena pyriformis. The migration, intracellular hormone content, and proliferation of Tetrahymena were investigated by microscope-assisted tracking analysis, flow cytometry, and a CASY TT cell counter, respectively. Depending on the length of linker sequence between the two GnRH-III monomers, the GnRH-III dimers had the opposite effect on Tetrahymena migration. [GnRH-III(CGFLG)]2 dimer had a slow, serpentine-like movement, while [GnRH-III(C)]2 dimer had a rather linear swimming pattern. All GnRH-III derivatives significantly induced cell growth after 6 h incubation. Endogenous histamine content was uniformly enhanced by Ac-SHDWKPG-NH2 and GnRH-III dimers, while some differences between the hormonal activities of GnRHs were manifested in their effects on intracellular levels of serotonin and endorphin. The GnRH peptides could directly affect Tetrahymena migration and proliferation in a structure-dependent manner, and they could indirectly regulate these reactions by paracrine/autocrine mechanisms. Present results support the theory that recognition ability and selectivity of mammalian hormone receptors can be deduced from a phylogenetically ancient level like the unicellular Tetrahymena.
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Dissertations / Theses on the topic "Gonadotrophin Hormone Releasing Hormone (GnRH)"

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Dorling, A. A. V. "Sex steroid regulation of gonadotrophin-releasing hormone (GnRH) neurons." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598603.

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Prior studies in the laboratory using quantitative in situ hybridisation and transgenic methodologies have shown that estrogen suppresses GnRH gene transcription and GnRH mRNA expression at times of negative feedback. Using the same approaches, I demonstrated that the positive feedback actions of estrogen were not coupled to alterations of GnRH gene expression. Recent RT-PCR studies identified estrogen receptor (ER)b transcripts in subpopulations of GnRH neurons in the mouse. To assess the presence of functional ERs in GnRH neurons, I undertook various gonadectomy-steroid replacement paradigms in several new transgenic reporter mouse line in which multiple estrogen response elements (EREs) drive the expression of LacZ (EREZ mice). Others have shown that this construct provides a functional reporter of ER-regulated gene transcription in vitro and I demonstrated its functionality in the uterus of EREZ mice. However, LacZ expression in the brain did not change in response to estrogen treatment and did not, therefore, enable us to evaluate the GnRH neurons. One possible reason for this failure is the recent discovery that the orphan nuclear receptors, termed estrogen receptor-related receptors (ERRs), constitutively transactivate EREs. To evaluate this further, I used in situ hybridisation to examine the topography of ERRa and ERRg expression in the mouse brain. I further demonstrated an estradiol-dependent decrease in ERRg expression in specific brain regions, suggesting a novel mechanism through which estradiol may regulate gene expression in the brain. Finally, I examined the negative feedback actions of estrogen upon GnRH neurons by evaluating LH levels and GnRH mRNA expression in knockout mice lacking either ERa or ERb.
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Hoo, L. C., and 何麗莊. "Transcriptional regulation of the human gonadotropin-releasing hormone(GnRH) II and GnRH receptor genes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29297011.

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Meyer, Colette. "Characterisation of the direct antiproliferative effects of a gonadotrophin-releasing hormone analogue." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6476.

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Gonadotrophin-releasing hormone (GnRH) can inhibit proliferation of multiple reproductive tissue cancer cell lines through direct interaction with GnRH receptors (GnRHR) on tumour cells. GnRH analogues may therefore have a role in treating some cancers. The signalling pathways associated with these inhibitory effects are poorly defined, and characterising them may help to understand therapeutic sensitivity. To elucidate these pathways, transcriptomic and proteomic approaches were used to compare the effects of the GnRH agonist Triptorelin in responsive GnRHR-transfected HEK293 cells (SCL60) and unresponsive (HEK293) cells both in vitro for up to 24h and in vivo for up to 7 days. Gene expression profiling demonstrated that SCL60 gene expression was temporally regulated with Triptorelin treatment, with expression of some genes increased at one time point but decreased at another. Early and mid-phase gene expression changes comprised mainly transcription factors and late changes included the hormonal signalling component CGA. Pathway analysis implicated mitogen-activated protein kinase and cell cycle pathways, supporting the detection of G2/M arrest. Signalling effects within SCL60 xenografts, 4 and 7 days following Triptorelin treatment, were investigated using a phosphoproteomic antibody array. Changes included cell cycle and apoptosis regulators, as well as cell surface receptors and NFκB signalling pathway members. Reverse-phase protein arrays and western blotting also showed that pAkt was decreased and pNFκB-p65 was increased after Triptorelin treatment in vitro. An NFκB inhibitor enhanced the anti-proliferative effect of Triptorelin in SCL60 cells in vitro, suggesting that NFκB acts as a survival factor in the response to GnRHR stimulation. A range of GnRHR expression was observed in breast cancer tumours by immunohistochemistry, and on average GnRHR expression was significantly higher in the Triple Negative Phenotype (TNP) subgroup and in grade 3 tumours. A GnRHR-transfected breast cancer cell line, MCF7-h14, was developed. Despite this expressing a similar level of GnRHR to responsive SCL60 cells, MCF7-h14 cells were not inhibited by GnRHR activation, indicating that a high level of GnRHR is insufficient for the antiproliferative effects of Triptorelin.
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Stavrou, Emmanouil. "Regulation of FOXO transcription factors by gonadotropin-releasing hormone." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5686.

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G protein-coupled receptors (GPCRs) are a large family of trans-membrane receptors that transmit signals from extracellular stimuli to target intracellular signal transduction pathways. The gonadotropin-releasing hormone receptor (GnRH-R) is a GPCR which binds the decapeptide GnRH. In the pituitary gonadotrope, GnRH stimulates gonadotropin (LH and FSH) biosynthesis and secretion to regulate reproduction. GnRH and the GnRH-Rs are also present in many extra-pituitary tissues, although their role at these sites remains largely undetermined. GnRH-Rs are known to recruit a diverse array of signalling pathway mediators in different cell-types. These include; Gq/11-PLCβ-IP3/DAG-Ca2+/PKC signalling, monomeric G-proteins and integrins to mediate cell adhesion and migration, the activation of the major members of the mitogen-activated protein kinase (MAPK) super-family (extracellular signal-regulated kinase (ERK), c-Jun N-terminal Kinase (JNK) and p38MAPK), and β-catenin and other mediators of the canonical Wnt signalling pathway. This thesis describes the regulation of Forkhead Box O (FOXO) transcription factors by GnRH. The mammalian FOXO transcription factors, FOXO1, FOXO3a and FOXO4, are emerging as an important family of proteins that modulate the expression of genes involved in cell-cycle regulation, induction of apoptosis, DNA damage repair and response to oxidative stress. In this thesis, emphasis is placed on delineating the novel role of FOXO transcription factors in mediating two important and widely-researched areas of GnRH biology. Firstly, the role of FOXO transcription factors in mediating cell-growth inhibition in response to GnRH treatment is assessed in a heterologous HEK293/GnRH-R expressing cell line. Secondly, the role of transcription factors in regulating luteinising hormone-β (LHβ)-subunit expression is investigated in the LβT2 gonadotrope cell line. Activation of the GnRH-R can inhibit cell proliferation and induce apoptosis in certain tumour-derived cell lines. Several studies have reported that these events can occur as a result of changes in the expression profiles of specific cell-cycle regulatory and apoptotic genes, many of which are FOXO-target genes, including GADD45, FasL, p21Cip1 and p27Kip1. In this thesis, a role for FOXOs in targeting the expression of several of these genes in response to GnRH is assessed, highlighting a specific role for FOXO3a in mediating GADD45 and FasL expression. The signalling mechanisms through which FOXO3a regulates GADD45 expression in response to GnRH is also described. Finally, a stable FOXO3a-knock-down cell line was generated in order to further examine FOXO3a involvement in GnRH-induced cell-growth inhibition. GnRH is an essential regulator of the reproductive process by stimulating the synthesis of LH and FSH in pituitary gonadotropes, thereby regulating gametogenesis and steroidogenesis. Diverse signalling pathways have been reported to regulate LHβ-subunit expression in response to GnRH, including the ERK/JNK/p38MAPK cascades and factors such as Egr1, SF1 and β-catenin. In the second part of this thesis, the role of FOXOs in regulating LHβ-subunit expression in response to GnRH is described. The data presented suggests that GnRH can regulate LHβ-subunit expression through both indirect and direct FOXO3a-mediated mechanisms. Firstly, FOXO3a was found to regulate Egr1 expression to indirectly target LHβ-promoter activity. Secondly, a role for β-catenin as a FOXO3a co-factor to directly regulate LHβ-subunit expression, together with Egr1 and SF1, is also proposed. FOXO3a expression and sub-cellular localisation was assessed and demonstrated in LβT2 cells and in adult human male pituitary sections. The research presented in this thesis adds to the diversity of signalling pathways and mediators that GnRH can target in different cellular backgrounds in order to mediate a variety of cellular processes. The antiproliferative and apoptotic effects of GnRH on tumour-derived cell lines are well-documented, and this research highlights a novel role for FOXO3a in mediating these events. The regulation of gonadotropin synthesis remains an important topic of research, and the novel implication of FOXO3a in mediating LHβ-subunit expression adds further complexity to gonadotrope physiology.
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Forsdike, Rachel Anne. "In utero development of sexually dimorphic gonadotrophin-releasing hormone (GnRH) secretion in sheep." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620917.

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曾美好 and May-ho Tsang. "Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) secretion and gene expression in a GnRH neuronal cell line." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31213698.

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Tsang, May-ho. "Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) secretion and gene expression in a GnRH neuronal cell line /." Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17095219.

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Wormald, Patricia J. "GnRH and neuropeptide regulation of gonadotropin secretion from cultured human pituitary cells." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27168.

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Gonadotropin-releasing hormone (GnRH) and its superactive analogues are currently being used in the treatment of a number of endocrine disorders, such as endometriosis, precocious puberty, infertility and prostatic cancer. Selection of these analogues for clinical use have been previously based on their activities in animal models. This thesis has therefore investigated the binding characteristics of the human GnRH receptor, in comparison to those of the rat receptor, as well as the activities of a number of GnRH analogues for stimulating luteinising hormone (LH) and follicle stimulating hormone (FSH) secretion from cultured human pituitary cells. The establishment of a human pituitary bioassay system has further made possible the investigation of the direct regulatory roles of GnRH and other neuropeptides in man. To date, such studies in man have been performed in vivo and are thus complicated by the simultaneous interactions of numerous modulators.
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Corchuelo, Chavarro Sheryll Yohana [UNESP]. "GnRH/GnIH e seus receptores no sistema olfato-retinal de zebrafish." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/134047.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O hormônio liberador de gonadotropina (GnRH) é um dos fatores chaves na regulação neuroendócrina da reprodução dos vertebrados. Alguns peixes apresentam três variantes do GnRH: o GnRH1 envolvido na secreção de gonadotropinas, o GnRH2 que regula o comportamento alimentar e sexual e o GnRH3 expresso no bulbo olfatório e o nervo terminal cujas fibras nervosas inervam a retina e o epitélio olfatório. O zebrafish possui duas variantes do GnRH (GnRH2 e GnRH3), sendo o GnRH3 a variante hipofisiotrófica. Estudos mostram possível envolvimento do GnRH no sistema olfato-retinal. No sistema olfatório o GnRH regula a sensibilidade na detecção de alimento, o reconhecimento intra e interespecífico, entre outros. Na retina, o GnRH3 pode estar envolvido na acuidade visual e do processamento de informação da retina. Existem estudos que reportam a presença de receptores de GnRH em diferentes camadas da retina, no entanto ainda não é clara a presença de receptores no epitélio olfatório. Neste contexto, no presente estudo analisamos a localização do gnrh2, gnrh3 e seus receptores (gnrhr1,2,3 e 4) e do gnih (hormônio inibidor de gonadotropinas) no epitélio olfatório, a retina e o bulbo olfatório de machos e fêmeas adultos e comparamos a expressão destes genes em fêmeas em diferentes estágios de maturação gonadal. Para tanto, o RNA total do epitélio olfatório, retina, bulbo olfatório, cérebro e gônadas foi extraído. Com base na sequência dos genes gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3 e gnrhr4, primers forward e reverse foram desenhados para RT-PCR e qPCR. Sondas para a hibridização in situ também foram construídas para verificar os sítios de expressão destas moléculas no epitélio olfatório, retina e gônadas. Imunohistoquímica com os anticorpos anti-GnRH3 (BB8 e GF6) foram realizadas para localizar a proteína do GnRH3 nos tecidos analisados. O presente estudo apresenta um panorama da expressão do sistema...
The gonadotropin releasing hormone (GnRH) is one of the key factors involved in the neuroendocrine regulation of vertebrate reproduction. Some fish species have three GnRH variants: GnRH1 involved in gonadotropin secretion, GnRH2 regulating food and sexual behaviors and the GnRH3 which is expressed in the olfactory bulb and terminal nerve whose fibers innervate the retina and the olfactory epithelium. Two GnRH variants (GnRH2 and GnRH3) are present in the zebrafish, in which GnRH3 acts as the hypophisiotrophic variant. Recent studies have been showing the role of GnRH in the olfactory-retinal system. In the olfactory system, GnRH regulates food detection, and intra and interspecific recognition. In retina, GnRH3 may be involved in visual acuity modulation and retinal processing information. Moreover, studies have reported the presence of GnRH receptors in the retina, but not yet in the zebrafish olfactory epithelium. Therefore, the current study analyzed the presence of GnRH2, GnRH3 and its receptors (GnRH-R1,2,3 and 4) and GnIH (gonadotropin inhibitory hormone) in the olfactory epithelium, olfactory bulb, retina and in gonads of adult zebrafish. We also compared the expression of these genes during the different stages of ovarian maturation in zebrafish. For that, total RNA of the olfactory epithelium, olfactory bulb, retina and gonads was extracted with the PureLink® RNA Mini Kit(Ambion®). RT-PCR and qPCR analysis were performed using forward and reverse primers for gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3, gnrhr4 for . Probes for in situ hybridization were constructed to verify the expression sites of these molecules in the olfactory epithelium, retina, and gonads. Immunohistochemistry usinganti-GnRH3 antibodies (BB8 and GF6) were performed to identify the GnRH3 protein in these tissues. The current study presents a general expression view of GnRH/GnIH and their receptors in the olfactory epithelium-olfactory bulb-retinal axis during ...
FAPESP: 2014/02481-9
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Corchuelo, Chavarro Sheryll Yohana. "GnRH/GnIH e seus receptores no sistema olfato-retinal de zebrafish /." Jaboticabal, 2015. http://hdl.handle.net/11449/134047.

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Orientador: Laura Satiko Okada Nakaghi
Coorientador: Rafael Henrique Nóbrega
Banca: Elisabeth Criscuolo Urbinati
Banca: Matias Pandolfi
Resumo: O hormônio liberador de gonadotropina (GnRH) é um dos fatores chaves na regulação neuroendócrina da reprodução dos vertebrados. Alguns peixes apresentam três variantes do GnRH: o GnRH1 envolvido na secreção de gonadotropinas, o GnRH2 que regula o comportamento alimentar e sexual e o GnRH3 expresso no bulbo olfatório e o nervo terminal cujas fibras nervosas inervam a retina e o epitélio olfatório. O zebrafish possui duas variantes do GnRH (GnRH2 e GnRH3), sendo o GnRH3 a variante hipofisiotrófica. Estudos mostram possível envolvimento do GnRH no sistema olfato-retinal. No sistema olfatório o GnRH regula a sensibilidade na detecção de alimento, o reconhecimento intra e interespecífico, entre outros. Na retina, o GnRH3 pode estar envolvido na acuidade visual e do processamento de informação da retina. Existem estudos que reportam a presença de receptores de GnRH em diferentes camadas da retina, no entanto ainda não é clara a presença de receptores no epitélio olfatório. Neste contexto, no presente estudo analisamos a localização do gnrh2, gnrh3 e seus receptores (gnrhr1,2,3 e 4) e do gnih (hormônio inibidor de gonadotropinas) no epitélio olfatório, a retina e o bulbo olfatório de machos e fêmeas adultos e comparamos a expressão destes genes em fêmeas em diferentes estágios de maturação gonadal. Para tanto, o RNA total do epitélio olfatório, retina, bulbo olfatório, cérebro e gônadas foi extraído. Com base na sequência dos genes gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3 e gnrhr4, primers forward e reverse foram desenhados para RT-PCR e qPCR. Sondas para a hibridização in situ também foram construídas para verificar os sítios de expressão destas moléculas no epitélio olfatório, retina e gônadas. Imunohistoquímica com os anticorpos anti-GnRH3 (BB8 e GF6) foram realizadas para localizar a proteína do GnRH3 nos tecidos analisados. O presente estudo apresenta um panorama da expressão do sistema...
Abstract: The gonadotropin releasing hormone (GnRH) is one of the key factors involved in the neuroendocrine regulation of vertebrate reproduction. Some fish species have three GnRH variants: GnRH1 involved in gonadotropin secretion, GnRH2 regulating food and sexual behaviors and the GnRH3 which is expressed in the olfactory bulb and terminal nerve whose fibers innervate the retina and the olfactory epithelium. Two GnRH variants (GnRH2 and GnRH3) are present in the zebrafish, in which GnRH3 acts as the hypophisiotrophic variant. Recent studies have been showing the role of GnRH in the olfactory-retinal system. In the olfactory system, GnRH regulates food detection, and intra and interspecific recognition. In retina, GnRH3 may be involved in visual acuity modulation and retinal processing information. Moreover, studies have reported the presence of GnRH receptors in the retina, but not yet in the zebrafish olfactory epithelium. Therefore, the current study analyzed the presence of GnRH2, GnRH3 and its receptors (GnRH-R1,2,3 and 4) and GnIH (gonadotropin inhibitory hormone) in the olfactory epithelium, olfactory bulb, retina and in gonads of adult zebrafish. We also compared the expression of these genes during the different stages of ovarian maturation in zebrafish. For that, total RNA of the olfactory epithelium, olfactory bulb, retina and gonads was extracted with the PureLink® RNA Mini Kit(Ambion®). RT-PCR and qPCR analysis were performed using forward and reverse primers for gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3, gnrhr4 for . Probes for in situ hybridization were constructed to verify the expression sites of these molecules in the olfactory epithelium, retina, and gonads. Immunohistochemistry usinganti-GnRH3 antibodies (BB8 and GF6) were performed to identify the GnRH3 protein in these tissues. The current study presents a general expression view of GnRH/GnIH and their receptors in the olfactory epithelium-olfactory bulb-retinal axis during ...
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Books on the topic "Gonadotrophin Hormone Releasing Hormone (GnRH)"

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Organon Round Table Conference (3rd 1992 Paris, France). GnRH, GnRH analogs, gonadotropins, and gonadal peptides: The proceedings of the third Organon Round Table Conference, Paris, 1992. London: Parthenon Pub. Group, 1993.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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World, Congress on Fertility and Sterility (15th 1995 Bologna Italy). Treatment with GnRH analogs: Controversies and perspectives : the proceedings of a satellite symposium of the 15th World Congress on Fertility and Sterility held in Bologna, Italy, 15-16 September 1995. New York: Parthenon Pub. Group, 1996.

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Gillespie, Julia M. A. Melatonin mediated regulation of gonadotropin-releasing hormone (GnRH): Role of melatonin receptors and circadian rhythms. Ottawa: National Library of Canada, 2002.

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Ferring Symposium on Brain and Pituitary Peptides (3rd 1985 Noordwijk, Netherlands). Pulsatile GnRH 1985: Proceedings of the 3rd Ferring Symposium, Noordwijk, September 11-13, 1985. Edited by Coelingh Bennink, Herman Jan Tymen, 1943-. Haarlem: Ferring, 1985.

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Elgendy, Manal. Minimising the dose of gonadotrophin releasing hormone agonist [GnRHa] and recombinant follicle stimulating hormone [FSH] used for controlled ovarian hyperstimulation in in-vitro fertilisation. Birmingham: University of Birmingham, 2001.

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Goodman, Stephanie Robin. Effects of gonadotrophin releasing hormone on growth hormone release in the rat. [New Haven, Conn: s.n.], 1993.

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International Symposium on GnRH Analogues in Cancer and Human Reproduction (8th 2005 Salzburg, Austria). GnRH analogs in human reproduction. London: Taylor & Francis, 2005.

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Book chapters on the topic "Gonadotrophin Hormone Releasing Hormone (GnRH)"

1

Colao, Annamaria, and Claudia Pivonello. "Gonadotropin Releasing Hormone (GnRH)." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5110-1.

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Colao, Annamaria, and Claudia Pivonello. "Gonadotropin Releasing Hormone (GnRH)." In Endocrine Pathology, 339–40. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5110.

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Braden, Tim D., and P. Michael Conn. "Gonadotropin Releasing Hormone and Its Actions." In Modes of Action of GnRH and GnRH Analogs, 26–54. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_2.

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Karsch, Fred J., Suzanne M. Moenter, and Alain Caraty. "The Preovulatory Surge of Gonadotropin Releasing Hormone." In Modes of Action of GnRH and GnRH Analogs, 241–55. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_16.

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Marshall, John C., Alan C. Dalkin, and Daniel J. Haisenleder. "Regulation of Gonadotropin Gene Expression by Gonadotropin Releasing Hormone." In Modes of Action of GnRH and GnRH Analogs, 55–66. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_3.

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Park, Ok-Kyong, Sajiv Gugneja, and Kelly E. Mayo. "Gonadotropin Releasing Hormone Gene Expression During the Rat Reproductive Cycle." In Modes of Action of GnRH and GnRH Analogs, 223–40. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_15.

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Bremner, William J., Carrie J. Bagatell, and Robert A. Steiner. "Gonadotropin Releasing Hormone Antagonist Plus Testosterone: A Potential Male Contraceptive." In Modes of Action of GnRH and GnRH Analogs, 322–31. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_21.

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Wierman, Margaret E., Wei Sun, Chun Wang, David F. Gordon, and William W. Wood. "Control of Rat Gonadotropin Releasing Hormone Promoter Activity in Placental Cells." In Modes of Action of GnRH and GnRH Analogs, 106–15. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_7.

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Mann, David R., Kenneth G. Gould, and Kim Wallen. "Use of Gonadotropin Releasing Hormone Analogs to Influence Sexual and Behavioral Development." In Modes of Action of GnRH and GnRH Analogs, 347–69. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_23.

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Hall, Janet E., Todd D. Brodie, Tom M. Badger, Jean Rivier, Wylie Vale, P. Michael Conn, and William F. Crowley. "Physiologic Effects of a Gonadotropin Releasing Hormone Antagonist in Normal Women." In GnRH Analogues in Reproduction and Gynecology, 77–88. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0721-8_9.

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Conference papers on the topic "Gonadotrophin Hormone Releasing Hormone (GnRH)"

1

Ohlsson, M., A. J. W. Hsueh, and T. Ny. "HORMONE REGULATION OF THE FIBRINOLYTIC SYSTEM IN THE OVARY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644389.

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In the ovary, the release of oocytes from graafian follicles during hormone-induced ovulation has been found to be associated with substantial increases in follicular plasminogen activator (PA) activity. Most of the PA activity comes from the granulosa cells that have been shown to produce tPA, uPA as well as the type-1 PA-inhibitor,(PAI-1).We have studied the molecular mechanism of follicle stimulating hormone (FSH) and gonadotropin releasing hormone (GnRH) on the synthesis of tPA in primary cultures of rat granulosa cells. FSH and GnRH were both found to induce tPA in granulosa cells in a time and dose dependent manner. The effect of FSH and GnRH on the levels of tPA mRNA was also studied by northern and slot blot hybridizations. FSH and GnRH were both found to increase the level of tPA mRNA. The stimulation was up to 18 -fold compared to untreated cells.The induction of tPA mRNA by FSH and GnRH was additive and the time courses of the stimulation by the hormones differed, suggesting that different cellular mechanisms are involved. Consistent with the ability of FSH to activate the cAMP dependent protein kinase A pathway, the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine further enhanced the FSH induction of tPA mRNA.GnRH is known to activate the phospholipid-dependent protein kinase C pathway. Likewise the effect of GnRH can be mimicked by the kinase C activator, phorbol myristate acetate.It is concluded that FSH and GnRH regulates tPA production by differnt molecular mechanisms, and that the increase in tPA activity is mediated via an increase in the levels tPA mRNA. Since both gonadotropins and GnRH cause ovulation in hyposectomized animals, similar stimulatory actions of these hormones on the tPA activity suggest a correlative relationship between this enzyme and the ovulatory process.
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Biniari, Georgia, Agathi Nteli, Carmen Simal, Christos Markatos, Vlasios Karageorgos, Alexios Vlamis-Gardikas, George Liapakis, and Theodore Tselios. "Design and Synthesis of Gonadotropin Releasing Hormone (GnRH) Peptide Analogues Conjugated with Anthraquinone for Selective Immunosuppression." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps/36eps.2022.065.

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Kim, HJ, MH Lee, JE Lee, SH Park, ES Lee, Y.-J. Kang, JH Lee, et al. "Abstract P1-12-09: The oncologic effect of a gonadotropin releasing hormone (GnRH) agonist for ovarian protection during breast cancer chemotherapy." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p1-12-09.

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Yoon, TI, HJ Kim, JH Yu, G. Sohn, BS Ko, JW Lee, BH Son, and SH Ahn. "Abstract P5-13-06: Concurrent gonadotropin-releasing hormone (GnRH) agonist administration with chemotherapy improves neoadjuvant chemotherapy responses in young premenopausal breast cancer patients." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-13-06.

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Wu, Hsien-Ming, Angel Chao, Tzu-Hao Wang, Hsin-Shih Wang, Hong-Yuan Huang, Chyi-Long Lee, Yung-Kuei Soong, and Peter C. K. Leung. "Abstract 3018: Gonadotropin-releasing hormone type II (GnRH-II) agonist regulates the invasiveness of endometrial cancer cells through GnRH-I receptor and mitogen-activated protein kinases (MAPKs)-dependent activation of matrix metalloproteinase (MMP)-2." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3018.

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Sand, Sharon R., Catherine Klifa, Michael F. Press, Malcolm Pike, Giske Ursin, Darcy Spicer, Lalit Vora, et al. "Abstract 3557: Reduced ovarian hormones & reduced mammographic & MRI determined breast density inBRCAcarriers following a hormonal chemo-prevention regimen of gonadotropin releasing hormone agonist (GnRHA) & low-dose add-back estrogen & testosterone." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3557.

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Reinisch, M., S. Seiler, T. Hauzenberger, S. Schmatloch, HJ Strittmatter, DM Zahm, C. Thode, et al. "Abstract PD7-10: Male-GBG54: A prospective, randomised multi-centre phase II study evaluating endocrine treatment with either tamoxifen +/- gonadotropin releasing hormone analogue (GnRHa) or an aromatase inhibitor + GnRHa in male breast cancer patients." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-pd7-10.

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Cruz, MRS, E. Motta, EMK Silva, SG Bernardo, and AN Atallah. "P5-23-04: Gonadotrophin-Releasing Hormone Analogues for Ovarian Function Preservation in Women with Premenopausal Breast Cancer Undergoing Adjuvant Chemotherapy: A Systematic Review and Meta-Analysis." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p5-23-04.

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Reports on the topic "Gonadotrophin Hormone Releasing Hormone (GnRH)"

1

Xu, Dan, Xueying Zhou, Junfei Wang, Xi Cao, and Tao Liu. The Value of Urinary Gonadotropins in the Diagnosis of Central Precocious Puberty: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0076.

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Review question / Objective: Precocious puberty is defined as the onset of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys. It can be differentiated into central precocious puberty (CPP) and peripheral precocious puberty, and it is more common in girls than in boys. CPP may result in a decreased final adult height, an early age at menarche, and psychological and health problems in adulthood. Gonadotropin-releasing hormone (GnRH) GnRH stimulation test has been indispensable in the diagnosis of CPP. GnRH stimulation test is not only invasive, time-consuming and expensive, but also sometimes difficult to have patients cooperate. Nocturnal urinary LH and FSH can represent gonadotropin excretion in children with normal and early puberty. And urinary sample collection and evaluation are more convenient, more acceptable, cheaper, and noninvasive. This meta-analysis aims to assess the value of first-voided urinary luteinizing hormone (LH) and the ratio of urinary luteinizing hormone and follicle-stimulating hormone (FSH) in the diagnosis of female CPP and to compare the accuracy between urinary gonadotropins and serum GnRH-stimulated gonadotropins.
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Gu, Li, Xurui Li, and Wentao Liu. Adverse cardiovascular effect following Gonadotropin-releasing Hormone (GnRH) antagonist versus GnRH agonist for Prostate Cancer Treatment: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0009.

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Yaron, Zvi, Abigail Elizur, Martin Schreibman, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon piceus) and the Striped Bass (Morone saxatilis). United States Department of Agriculture, January 2000. http://dx.doi.org/10.32747/2000.7695841.bard.

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Both the genes and cDNA sequences encoding the b-subunits of black carp LH and FSH were isolated, cloned and sequenced. Sequence analysis of the bcFSHb and LHb5'flanking regions revealed that the promoter region of both genes contains canonical TATA sequences, 30 bp and 17 bp upstream of the transcription start site of FSHb and LHb genes, respectively. In addition, they include several sequences of cis-acting motifs, required for inducible and tissue-specific transcriptional regulation: the gonadotropin-specific element (GSE), GnRH responsive element (GRE), half sites of estrogen and androgen response elements, cAMP response element, and AP1. Several methods have been employed by the Israeli team to purify the recombinant b subunits (EtOH precipitation, gel filtration and lentil lectin). While the final objective to produce pure recombinantGtH subunits has not yet been achieved, we have covered much ground towards this goal. The black carp ovary showed a gradual increase in both mass and oocyte diameter. First postvitellogenic oocytes were found in 5 yr old fish. At this age, the testes already contained spermatozoa. The circulating LH levels increased from 0.5 ng/ml in 4 yr old fish to >5ng/ml in 5 yr old fish. In vivo challenge experiments in black carp showed the initial LH response of the pituitary to GnRH in 4 yr old fish. The response was further augmented in 5 yr old fish. The increase in estradiol level in response to gonadotropic stimulation was first noted in 4 yr old fish but this response was much stronger in the following year. In vivo experiments on the FSHb and LHb mRNA levels in response to GnRH were carried out on common carp as a model for synchronom spawning cyprinids. These experiments showed the prevalence of FSHP in maturing fish while LHP mRNA was prevalent in mature fish, especially in females. The gonadal fat-pad was found to originate from the retroperitoneal mesoderm and not from the genital ridge, thus differing from that reported in certain amphibians This tissue possibly serves as the major source of sex steroids in the immature black carp. However, such a function is taken over by the developing gonads in 4 yr old fish. In the striped bass, we described the ontogeny of the neuro-endocrine parameters along the brain-pituitary-gonadal axis during the first four years of life, throughout gonadal development and the onset of puberty. We also described the responsiveness of the reproductive axis to long-term hormonal manipulations at various stages of gonadal development. Most males reached complete sexual maturity during the first year of life. Puberty was initiated during the third year of life in most females, but this first reproductive cycle did not lead to the acquisition of full sexual maturity. This finding indicates that more than one reproductive cycle may be required before adulthood is reached. Out of the three native GnRHs present in striped bass, only sbGnRH and cGnRH II increased concomitantly with the progress of gonadal development and the onset of puberty. This finding, together with data on GtH synthesis and release, suggests that while sbGnRH and cGnRH II may be involved in the regulation of puberty in striped bass, these neuropeptides are not limiting factors to the onset of puberty. Plasma LH levels remained low in all fish, suggesting that LH plays only a minor role in early gonadal development. This hypothesis was further supported by the finding that experimentally elevated plasma LH levels did not result in the induction of complete ovarian and testicular development. The acquisition of complete puberty in 4 yr old females was associated with a rise in the mRNA levels of all GtH subunit genes, including a 218-fold increase in the mRNA levels of bFSH. mRNA levels of the a and PLH subunits increased only 11- and 8-fold, respectively. Although data on plasma FSH levels are unavailable, the dramatic increase in bFSH mRNA suggests a pivotal role for this hormone in regulating the onset and completion of puberty in striped bass. The hormonal regulation of the onset of puberty and of GtH synthesis and release was studied by chronic administration of testosterone (T) and/or an analog of gonadotropin-releasing hormone (G). Sustained administration of T+G increased the mRNA levels of the PLH subunit to the values characteristic of sexually mature fish, and also increased the plasma levels of LH. However, these changes did not result in the acceleration of sexual maturation. The mRNA levels of the bFSH subunit were slightly stimulated, but remained about 1/10 of the values characteristic of sexually mature fish. It is concluded that the stimulation of FSH gene expression and release does not lead to the acceleration of sexual maturity, and that the failure to sufficiently stimulate the bFSH subunit gene expression may underlie the inability of the treatments to advance sexual maturity. Consequently, FSH is suggested to be the key hormone to the initiation and completion of puberty in striped bass. Future efforts to induce precocious puberty in striped bass should focus on understanding the regulation of FSH synthesis and release and on developing technologies to induce these processes. Definite formulation of hormonal manipulation to advance puberty in the striped bass and the black carp seems to be premature at this stage. However, the project has already yielded a great number of experimental tools of DNA technology, slow-release systems and endocrine information on the process of puberty. These systems and certain protocols have been already utilized successfully to advance maturation in other fish (e.g. grey mullet) and will form a base for further study on fish puberty.
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