Hormonal Regulation of Pituitary Gonadotropin Gene Expression

Counis, Raymond; Corbani, Maïthé; Starzec, Anna; Jutisz, M

doi:10.1007/978-1-4684-5131-3_12

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…The synthesis of mammalian gonadotropins is regu lated primarily by GnRH (being mediated by calcium, cAMP and PKC) and gonadal steroids [13][14][15][16]. Estrogenresponsive elements have been identified in the promoter region of the salmon GtH II|3 gene which confer a stimula tory effect on its expression, and it is suggested that one of these may interact with other transcription factors such as those originating from the GnRH induced signals [17,18].…”

Section: Introductionmentioning

confidence: 99%

Differential Effects of Gonadotropin-Releasing Hormone, Dopamine and Somatostatin and Their Second Messengers on the mRNA Levels of Gonadotropin IIβ Subunit and Growth Hormone in the Teleost Fish, Tilapia

Melamed

Gur

Elizur³

et al. 1996

Neuroendocrinology

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In cultured pituitary cells of tilapia, gonadotropin-releasing hormone (GnRH; IO11M 4-24 h), elevation of cyclic AMP (by 10 µM forskolin or 0.2 mM3-isobutyl-1-methylxanthine: IBMX 0.5-36 h) or activation of protein kinase C (PKC; by 12.5 nM tetradecanoyl phorbol-13-acetate: TPA, 0.5–24 h) all increased gonadotropin (GtH) IIβ steady state mRNA levels by three- to fourfold. The involvement of PKA and PKC in the GnRH stimulatory effect on both GtH release and GtH IIβ mRNA levels was corroborated by use of the PKA and PKC inhibitors, H89 and GF109203X, respectively (100 nM) which attenuated the GnRH effect. Incubation with actinomycin D (8 µM, 4–21 h) after preexposure for 24 h to either forskolin (10 µM) or TPA (12.5 nM), revealed that rates of transcript degradation were slower in forskolin-treated cells (T½ = 14.1 h) than in control or TPA-treated cells (T½ = 8.47 or 8.38 h), suggesting a stabilizing effect on the mRNA. Dopamine (DA; 10 µM, 4–36 h) had no apparent effect on steady state mRNA levels of GtH Ilβ, but reduced GtH release by as much as 75%. Steady state levels of growth hormone (GH) mRNA were not affected by exposure to GnRH (10 nM, 4–24 h), although GH release was more than doubled. Similarly, activation of PKC (by TPA 12.5 nM, 1.5–36 h), which was shown to be essential for the GnRH-stimulatory effect on GH release, did not alter levels of the GH transcript, but increased GH release by more than fivefold. DA (10 µM, 4–24 h) moderately increased GH transcript levels (160%) with similar kinetics but lower potency than direct elevation of cAMP (by 10 µM forskolin or 0.2 mM f IBMX, 0.5-36 h) which increased transcript levels by more than fourfold. The involvement of PKA in the DA effect was confirmed when the PKA inhibitor H89 (100 nM, 15 min prior to DA exposure) attenuated the DA effect on GH mRNA levels. Exposure of cells to actinomycin D (8 µM, 2–16 h) after treatment with forskolin (10 µM, 24 h) led to a slower rate of transcript degradation than in control cells (T½ = 6.5 h vs. T½ = 4.36 h), suggesting that cAMP also elicits a stabilizing effect on GH mRNA. Somatostatin (100 nM, 0.5-36 h) had no clear effect on GH transcript levels, but reduced GH release by as much as 90%. These results suggest that activation of either cAMP-PKA or PKC pathways can, possibly by different mechanisms, stimulate mRNA levels of the GtH IIβ gene, but that only the cAMP-PKA pathway stimulates GH mRNA levels. It would appear therefore that GnRH, although stimulating GH release, does not regulate GH transcription in this fish.

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Section: Introductionmentioning

confidence: 99%

Differential Effects of Gonadotropin-Releasing Hormone, Dopamine and Somatostatin and Their Second Messengers on the mRNA Levels of Gonadotropin IIβ Subunit and Growth Hormone in the Teleost Fish, Tilapia

Melamed

Gur

Elizur³

et al. 1996

Neuroendocrinology

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“…and FSH/?) result from post-translational maturation of precursors that are encoded by separate genes (Gharib et al, 1990;Counis and Jutisz, 1991). The expression of a and /?…”

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confidence: 99%

Effect of 4-MeSer-GnRH on the release and synthesis of gonadotropins in the female rat <i>in vivo</i>

Kochman¹,

Gajewska²,

Kochman³

et al. 1997

J. Anim. Feed Sci.

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The experiment was performed to confirm selective stimulation of FSH release by GnRH analog 4-MeSer-GnRH and to determine if analog can act on a, LH/? and prolactin gene expression. Our studies in vivo have shown that 4-MeSer-GnRH FSH releasing potency was less expressed than it was shown in our previous experiments and that this peptide did not affect LH release. GnRH analog inhibited both pituitary prolactin and LH/? mRNAs level but this effect was much more strongly expressed in case of prolactin mRNA. Such data point out a necessity of more detailed studies on the biological properties of 4-MeSer-GnRH.

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“…activin. and follistatin and gonadal ste roids [1][2][3][4][5]. In vivo studies on androgen-mediated regula tion of rat FSH|3 gene expression suggest that age, time elapsed since castration, simultaneous or delayed andro gen replacement, dose and mode of replacement are all critical factors in determining whether androgens stimu late.…”

Section: Introductionmentioning

confidence: 99%

Hormonal Regulation of Human Follicle-Stimulating Hormone-β Subunit Gene Expression: GnRH Stimulation and GnRH-Independent Androgen Inhibition

Kumar¹,

Low²

1995

Neuroendocrinology

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Previous studies from our laboratory demonstrated that chronic testosterone administration to castrated transgenic mice suppressed human follicle-stimulating hormone-β (FSHβ) mRNA levels transcribed from a human transgene to approximately 20% of control values. In the present study we used primary pituitary cultures prepared from the transgenic mice and in vivo experiments in hypogonadal (hpg) mice carrying the human transgene to assess the role of hypothalamic gonadotropin-releasing hormone (GnRH) in this inhibitory action. The levels of human FSHβ mRNA in monolayer cultures of pituitary cells were decreased by 24-hour treatments with 10 nM testosterone propionate or 5α-dihydrotestosterone to 13 and 26% of control values, respectively, in the absence of GnRH. For the in vivo experiments we introduced the 10-kb human FSHβ transgene into the hpg genetic background by selective crossbreeding. Daily injections of 1 µg GnRH for 14 days induced expression of the human FSHβ gene in male and female mice. Maximal effects were obtained by GnRH treatment of gonadectomized, hpg transgenic mice. Human FSHβ mRNA levels rose to approximately 4- or 10-fold that of control males and females, respectively. The stimulation was blocked completely by simultaneous administration of testosterone propionate in males and partially by estradiol in females. Pituitary content of immunoreactive FSH paralleled the mRNA changes. These data suggest that testosterone feedback inhibits the human FSHβ subunit gene directly at the pituitary gland in addition to the indirect mechanism of GnRH suppression. Furthermore, the in vitro data indicate that the suppression of human FSHβ gene expression is at least partly a direct androgen effect that does not require aromatization of testosterone to estradiol.

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Hormonal Regulation of Pituitary Gonadotropin Gene Expression

Cited by 5 publications

References 27 publications

Differential Effects of Gonadotropin-Releasing Hormone, Dopamine and Somatostatin and Their Second Messengers on the mRNA Levels of Gonadotropin IIβ Subunit and Growth Hormone in the Teleost Fish, Tilapia

Differential Effects of Gonadotropin-Releasing Hormone, Dopamine and Somatostatin and Their Second Messengers on the mRNA Levels of Gonadotropin IIβ Subunit and Growth Hormone in the Teleost Fish, Tilapia

Effect of 4-MeSer-GnRH on the release and synthesis of gonadotropins in the female rat <i>in vivo</i>

Hormonal Regulation of Human Follicle-Stimulating Hormone-β Subunit Gene Expression: GnRH Stimulation and GnRH-Independent Androgen Inhibition

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