Modulation of growth hormone (GH) secretion and GH mRNA levels by GH-releasing factor, somatostatin and secretagogues in cultured bovine adenohypophysial cells

Tanner, Jean-Paul; Davis, Scott K.; McArthur, N. H.; French, J. T.; Welsh, T. H.

doi:10.1677/joe.0.1250109

Cited by 29 publications

(10 citation statements)

References 16 publications

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“…59], In our culture system, SS had a direct inhibitory effect on GH mRNA levels, in agreement with some reports [54], but in contrast to others [53,60]. However, as mentioned above, we saw no effect of SS on basal Pit-1 mRNA levels.…”

Section: Discussionsupporting

confidence: 93%

“…Testosterone stimulates hypothalamic GHRH synthesis [40], which in turn stimu lates GH synthesis and secretion [51][52][53][54], We. as others [51][52][53][54], have seen that GHRH stimulates GH mRNA levels in vitro and we now report that this effect is also seen on Pit-1 mRNA levels. The somatotroph's response to GHRH involves the augmentation of cellular cAMP levels [53] and the GH gene contains a cAMP response element (CRE) [55].…”

Section: Discussionmentioning

confidence: 99%

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In vivo and in vitro Regulation of Pituitary Transcription Factor-1 (Pit-1) by Changes in the Hormone Environment

et al. 1996

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Pituitary transcription factor-1 (Pit-1 or GHF-1) is a transcription factor specific to the anterior pituitary and is involved in the expression and regulation of the growth hormone (GH), prolactin (PRL) and thyroid-stimulating hormone (TSH) β-subunit genes. The expression of these three genes can be modulated by changes in the hormone environment and it is thought that some of these effects are mediated through Pit-1, but little is known about the physiological regulation of this transcription factor. Therefore, we first asked whether Pit-1 gene expression is modified as a result of changes in the in vivo gonadal steroid environment and if this could be correlated with changes in GH and/or PRL mRNA levels. Secondly, we sought to determine if sex steroids affect the mRNA levels of these three peptides by acting at the level of the pituitary and whether these effects are androgen or estrogen mediated. Finally, how sex steroids modulate the response of these three genes to the hypothalamic neuropeptides growth hormone-releasing hormone (GHRH) and somatostatin (SS) was analyzed. To this end, we compared Pit-1 GH and PRL mRNA levels in the anterior pituitary of intact, castrated, and castrated testosterone-replaced adult male rats. In addition, primary cultures of adult male pituitaries were used to study the direct effects of both androgens and estrogens on Pit-1 GH, and PRL mRNA levels. In situ hybridization histochemistry was used to compare relative levels of Pit-1 GH and PRL mRNA. Densitometric analysis of the in vivo studies showed that castration resulted in a 57, 40 and 55% decline in Pit-1 GH and PRL mRNA signal levels, respectively. Furthermore, replacement with testosterone (T) at the time of castration completely prevented the decline in all three mRNA species (ANOVA: Pit-1 mRNA, p < 0.0001; GH mRNA, p < 0.0001; PRL mRNA, p < 0.0001). In vivo, both T (10^–7M) and estradiol (10^–9 M) were capable of stimulating Pit-1 mRNA and PRL mRNA levels, while dihydrotestosterone (DHT; 10^–7M) had no effect. There was no effect of any of these steroid treatments on GH mRNA levels in vitro. Addition of GHRH to the cultures increased GH mRNA levels, as well as those of Pit-1 and PRL, and SS had the opposite effect on GH mRNA levels. Whereas the GH response to GHRH was not significantly modified by exposure to sex steroids, the effect of SS was. The presence of sex steroids was capable of modifying the Pit-1 and PRL responses to both GHRH and SS. These results clearly indicate that changes in circulating levels of sex steroids modulate the expression of Pit-1 in the anterior pituitary and that these changes can be correlated with commensurate modifications in GH and PRL mRNA levels. Furthermore, the effect on both Pit-1 and PRL mRNA levels occurs, at least in part, at the level of the anterior pituitary and is an estrogen-receptor-mediated event. In contrast, the effects of gonadal steroids on GH mRNA levels are less direct and are most likely mediated at the level of the hypothalamus, as w...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

In vivo and in vitro Regulation of Pituitary Transcription Factor-1 (Pit-1) by Changes in the Hormone Environment

et al. 1996

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“…Similarly, SRIF inhibited GH secretion without affecting GH mRNA expression in primary human GH-secreting tumors cells (Davis et al 1989). In cultured bovine pituitary cells, SRIF was able to suppress GHRH-induced GH expression, but had no effect on untreated cells (Tanner et al 1990). Moreover, while sst2-specific and sst5-specific agonists suppressed GH secretion in human GH-secreting tumors, they did not affect GH transcription (Gruszka et al 2012).…”

Section: Gh Secretionmentioning

confidence: 91%

“…While direct inhibition of pituitary hormone transcription has yet to be definitively associated with SRIF signaling, as some studies demonstrate a SRIF-dependent decrease in GH mRNA levels (Sugihara et al 1993, Tsukamoto et al 1994, Acunzo et al 2008) others describe no change (Simard et al 1986, Davis et al 1989, Namba et al 1989, Tanner et al 1990, Gruszka et al 2007, and some even demonstrate upregulation of gene expression possibly reflecting a GH-rebound effect after termination of SRIF treatment; the latter exemplifies the importance of outcome measurement timing. SRIF did not affect GH mRNA expression, but did suppress intracellular GH protein levels and decreased GH secretion in primary rat anterior pituitary cells (Simard et al 1986).…”

Section: Gh Secretionmentioning

confidence: 99%

Somatostatin system: molecular mechanisms regulating anterior pituitary hormones

Eigler¹,

Ben-Shlomo²

2014

Journal of Molecular Endocrinology

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The somatostatin (SRIF) system, which includes the SRIF ligand and receptors, regulates anterior pituitary gland function, mainly inhibiting hormone secretion and to some extent pituitary tumor cell growth. SRIF-14 via its cognate G-protein-coupled receptors (subtypes 1-5) activates multiple cellular signaling pathways including adenylate cyclase/cAMP, MAPK, ion channel-dependent pathways, and others. In addition, recent data have suggested SRIF-independent constitutive SRIF receptor activity responsible for GH and ACTH inhibition in vitro. This review summarizes current knowledge on ligand-dependent and independent SRIF receptor molecular and functional effects on hormone-secreting cells in the anterior pituitary gland.

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“…Adenohypophyses were dissected from the neurohypophysis and adenohypophyseal cells were dispersed enzymatically as described previously (Welsh et al 1986, Tanner et al 1990). Dispersed cells from two steers were combined, plated in six-well plates, and cultured in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum for 4 days.…”

Section: Synthesis Of Lgnrh-iiimentioning

confidence: 99%

Evidence that lamprey GnRH-III does not release FSH selectively in cattle

Amstalden¹,

Zieba²,

Garcia³

et al. 2004

Reproduction

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Experiments were performed to test the hypothesis that lamprey GnRH-III (lGnRH-III) selectively releases FSH. Primary cultures of bovine adenohypophyseal cells were treated with mammalian GnRH (mGnRH) and lGnRH-III (10 29 , 10 28, 10 27and 10 26 M) or control media in Experiment 1. All doses of mGnRH and the two highest doses of lGnRH-III stimulated (P < 0.001) a non-selective release of LH and FSH. In Experiments 2 -4, Latin Square designs were utilized in vivo to examine whether physiological and hormonal milieu regulate putative selective effects of lGnRH-III. In Experiments 2 and 3, ovariectomized cows with basal levels of estradiol only (Experiment 2) or in combination with luteal phase levels of progesterone (Experiment 3) were injected with mGnRH and lGnRH-III (0.055, 0.11, 0.165 and 1.1 mg/kg body weight (BW) and saline. All doses of mGnRH released (P < 0.001) LH and FSH, but only the highest dose of lGnRH-III stimulated (P < 0.001) a non-selective release of both LH and FSH (Experiment 3). For Experiments 4A and 4B, intact, mid-luteal phase cows were injected with mGnRH and lGnRH-III (1.1 mg/kg BW; Experiment 4A), lGnRH-III (1.1 and 4.4 mg/kg BW; Experiment 4B) and saline. As before, mGnRH released (P < 0.001) both LH and FSH at all doses. In contrast, lGnRH-III at the highest dose released (P < 0.001) LH but not FSH. These findings suggest that lGnRH-III may act as a weak competitor for the mGnRH receptor and do not support the hypothesis that it selectively releases FSH in cattle.

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Modulation of growth hormone (GH) secretion and GH mRNA levels by GH-releasing factor, somatostatin and secretagogues in cultured bovine adenohypophysial cells

Cited by 29 publications

References 16 publications

In vivo and in vitro Regulation of Pituitary Transcription Factor-1 (Pit-1) by Changes in the Hormone Environment

In vivo and in vitro Regulation of Pituitary Transcription Factor-1 (Pit-1) by Changes in the Hormone Environment

Somatostatin system: molecular mechanisms regulating anterior pituitary hormones

Evidence that lamprey GnRH-III does not release FSH selectively in cattle

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