Effect of 17β-Estradiol on thyroliberin responsiveness in GH3/B6 rat prolactin cells

Brunet, N.; Gourdji, D.; Tixier‐Vidal, A.

doi:10.1016/0303-7207(80)90087-8

Cited by 25 publications

(10 citation statements)

References 32 publications

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“…There were no significant differences between results obtained after 10 to 48 h pretreatments with 178-estradiol, suggesting that pretreatment with 178-estradiol for 10 h would be sufficient to bring about an increase in TRH receptor number if this is indeed the factor responsible for the increased response. This differs from results obtained from tumoral (GH,) cells, in which pretreatment for 5 to 7 days with 17p-estradiol (4x lo8 M) is necessary to induce an increase of TRH binding sites (29). However, these results are in agreement with previous findings obtained in vivo (1) and from tumoral cells (5,29) indicating that 178-estradiol pretreatment increases the number of TRH binding sites.…”

Section: Figcontrasting

confidence: 56%

“…This differs from results obtained from tumoral (GH,) cells, in which pretreatment for 5 to 7 days with 17p-estradiol (4x lo8 M) is necessary to induce an increase of TRH binding sites (29). However, these results are in agreement with previous findings obtained in vivo (1) and from tumoral cells (5,29) indicating that 178-estradiol pretreatment increases the number of TRH binding sites. The increase in the number of apparently TRH-sensitive cells, as defined in this model, could also be explained by an increase in TRH receptor number.…”

Section: Figcontrasting

confidence: 56%

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In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture

Zhang

Chen

Kukstas

et al. 1990

J Neuroendocrinology

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Continuous cell perifusion and reverse hemolytic plaque assay have been used to show a regulatory action of 178-estradiol on lactotroph responsiveness to thyrotropin-releasing hormone (TRH) or dopamine (DA) in vifro. Lactotroph-enriched cell cultures were obtained from adult male rats after trypsinization and mechanical dissociation followed by separation on a continuous bovine Serum albumin gradient at unit gravity. After 7 days in culture, perifusion experiments showed that prolactin was continuously released and this release was increased by TRH and decreased by DA. Both TRH-induced secretion and DA-induced inhibition of prolactin release were dose-dependent with a half maximal effect obtained at 7 x lo-' M for TRH and at lo-' M for DA. It was shown by reverse hemolytic plaque assay that about 55% of the cells were plaque-forming (lysis of red blood cells) and were thus identified as prolactin-secreting cells. This was similar to a previous result obtained by immunofluorescent staining. Heterogeneity among lactotrophs with regard to the quantity of prolactin released was clearly shown by the varying plaque areas in all preparations. In order to make a quantitative analysis of the effect of 178-estradiol on TRH-stimulation and DAergic inhibition in these heterogeneous prolactin cells, they were divided into two groups: large plaques ( 2 3 x lo3 pm') constituted about 35% of all plaque-forming cells, and small plaques ( < 3 x l o 3 pm'), about 65%. Pretreatment with 178-estradiol (lo-' M) either for 10 h or 48 h markedly increased TRH-stimulated prolactin release and decreased the inhibitory effect of DA both in perifusion and reverse hemolytic plaque assay experiments. However, these pretreatments did not change the values of half maximum dose for TRH and DA. TRH transformed about 7% of the small plaques into large plaques and this proportion was increased to 25% after 178-estradiol treatment. On the contrary, DA and its more stable analogue bromocriptine increased the percentage of small plaques by 10% to 15% but this effect was decreased after 178-estradiol treatment. We conclude that: 1) Normal rat pituitary lactotrophs show heterogeneity with respect to their spontaneous release and responsiveness to TRH and DA; 2) pretreatment with 178-estradiol increases the response to TRH and decreases the response to DA without altering the doses at which they have half maximal effect; 3) there is no significant difference between the effect of 17fl-estradiol obtained after 10 h and after 48 h pretreatment.It has long been shown that estrogens play a modulatory role in the control of prolactin (PRL) secretion although its mode of action remains unclear. Pretreatment with 17B-estradiol has been shown to increase the number of thyrotropin-releasing hormone (TRH) binding sites in pituitary homogenates from female rats, whilst concomitantly enhancing the amount of PRL released in response to iv injection of TRH (1, 2). Similarly, in tumoral PRL e l l s in culture, the number of TRH binding sites and TRHinduced PRL...

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Section: Figcontrasting

confidence: 56%

Section: Figcontrasting

confidence: 56%

In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture

Zhang

Chen

Kukstas

et al. 1990

J Neuroendocrinology

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“…These cell lines are somatolactotrophs that secrete both PRL and growth hormone and in some cases proliferate on estrogen treatment (7)(8)(9). However, the response of these cell lines has been variable, with some investigators reporting no effect or negative effects of estrogen on proliferation (9)(10)(11)(12), whereas others reported estrogen-stimulated proliferation (13,14).…”

mentioning

confidence: 99%

Differential regulation by estrogens of growth and prolactin synthesis in pituitary cells suggests that only a small pool of estrogen receptors is required for growth

Chun

Gregg

Sarkar³

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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PR1 cells are a prolactin (PRL)-secreting cell line derived from a pituitary lactotroph tumor found in 17␤-estradiol-treated Fischer 344 rats. We examined the effect of estrogen on cell proliferation and PRL synthesis under various culture conditions. Estrogen, at extremely low concentrations, induces cell proliferation in this cell line, whereas antiestrogen inhibits proliferation. Interestingly, the proliferation response is much more sensitive than the PRL response because 0.01 pM estradiol or diethylstilbestrol induces half-maximal growth induction [Ϸ0.1% estrogen receptor (ER) occupancy is required], whereas 0.01 nM concentration is required for half-maximal PRL induction (Ϸ50% ER occupancy is required). The proliferation response is not as sensitive to antiestrogen as the PRL response, because 10 nM concentration of the pure antiestrogen ICI 182,780 could not inhibit 1 nM estradiol-or diethylstilbestrol-induced proliferation. The same concentration of ICI 182,780 decreased PRL secretion to 1% of estradiol-or diethylstilbestrol-induced prolactin secretion suggesting a possible dichotomy of ER control of proliferation and PRL synthesis. The K d of ER binding in these cells is about 3 ؋ 10 ؊11 M. These results with the PR1 cells extend previous studies in other estrogenregulated systems and suggest that only a small pool of ER is required for cell proliferation in contrast with the regulation of expression of specific genes. They also raise questions as to how a dimeric receptor functions when only one ligand site is occupied or when both an estrogen and an antiestrogen occupy one dimer.Estrogen is a physiological regulator of both replication and prolactin (PRL) synthesis in pituitary lactotrophs. Pituitaries of the Fischer 344 (F344) rat strain form tumors in response to 6-10 weeks of estrogen treatment (1-3). The GH3 cell line was derived from the radiation-induced MtT͞W5 transplantable pituitary tumor (4), and the GH4C1 cell line was subcloned from the GH3 cell line (5, 6). These cell lines are somatolactotrophs that secrete both PRL and growth hormone and in some cases proliferate on estrogen treatment (7-9). However, the response of these cell lines has been variable, with some investigators reporting no effect or negative effects of estrogen on proliferation (9-12), whereas others reported estrogen-stimulated proliferation (13, 14).In the above-mentioned research, replication was more sensitive than PRL synthesis to estrogen. GH4C1 pituitary tumor cell growth was 10-fold more sensitive to estrogen than PRL mRNA accumulation (14). GH3 cells showed maximum cell growth at 0.01 nM 17␤-estradiol (E2), whereas only half-maximal PRL production occurred at the same concentration (13). These data, although interesting, did not lead to any additional studies.We have studied the relationship between estrogen-induced cell proliferation and PRL expression by using a newly established pituitary cell line (PR1) from E2-treated F344 female rats (15). The cell growth response in this cell line is 1,000-fold mor...

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“…The effect of CRF on PRL release is not direct, however. As shown by others [4,8], we observed that in vitro, pituitary cells needed to be preincu bated in the presence of 17(i-estradiol in order to stimulate PRL secretion by CRF. Steroids have also been shown to mo dulate pituitary responsiveness toward other neurohormones.…”

Section: Discussionmentioning

confidence: 96%

Effect of Corticotropin-Releasing Factor on the Release and Synthesis of Prolactin

Morel

Enjalbert

Proulx³

et al. 1989

Neuroendocrinology

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Corticotropin-releasing factor (CRF) has been characterized on the basis of its intrinsic activity to release corticotropin from cultured rat anterior pituitary cells. Injected in intact rats, CRF increases adrenocorticotropic hormone (ACTH) release. Endogenous CRF-like immunoreactivity was detected in the cytoplasm and nucleus of corticotrophs. Using an antirat CRF serum, a similar location of CRF-like immunoreactivity was observed in lactotrophs: cytoplasmic matrix, secretory granules, nucleus and, to a lesser degree, the plasma membrane level were stained. One injection of CRF increased the plasma ACTH concentration 4-fold after 15 min, while plasma prolactin (PRL) increased 2.7-fold 5 min after injection. In vitro, incubation of female pituitary cells with rat CRF (10^–10–10^–8M) had no significant effect on PRL secretion. In contrast, after 4 days of in vitro pretreatment with 17β-estradiol (10^–9M), rat CRF stimulated PRL secretion by 42%. In situ hybridization of whole pituitary slices showed that rat CRF injection significantly increased the labeling of corticotrophs using an ACTH-cDNA probe, but had no significant effect on the labeling of lactotrophs using a PRL riboprobe. These results indicate that CRF is a factor which can modulate PRL release but not the synthesis of PRL.

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Effect of 17β-Estradiol on thyroliberin responsiveness in GH3/B6 rat prolactin cells

Cited by 25 publications

References 32 publications

In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture

In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture

Differential regulation by estrogens of growth and prolactin synthesis in pituitary cells suggests that only a small pool of estrogen receptors is required for growth

Effect of Corticotropin-Releasing Factor on the Release and Synthesis of Prolactin

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