Differential Effect of Age on Transforming Growth Factor-β1 Inhibition of Prolactin Gene Expression<i>Versus</i>Secretion in Rat Anterior Pituitary Cells<sup>1</sup>

Tan, Sai-Koong; Wang, Fung-Fang; Pu, Hsiao‐Fung; Liu, Tsuei-Chu

doi:10.1210/endo.138.3.4996

Cited by 11 publications

(2 citation statements)

References 51 publications

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“…The sensitivity of the assay was 30 pg/tube/ml assay volume. The intra- and interassay coefficients of variation were 9.0 and 14.5%, respectively [27]. …”

Section: Methodsmentioning

confidence: 99%

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Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Pu¹,

Tan²,

Chen³

et al. 1999

Neuroendocrinology

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Acetylcholine (ACh), synthesized in the pituitary, can act locally to modulate pituitary function. We used rat primary anterior pituitary (AP) cells to investigate how ACh affects pituitary prolactin (PRL) secretion in the presence or absence of known PRL regulators: thyrotropin-releasing hormone (TRH), 17β-estradiol (E₂) and triiodothyronine (T₃). Cultured AP cells were prepared from ovariectomized rats and pretreated with diluent, 0.6 nM E₂, 10 nM T₃, or E₂ plus T₃ for 5 days, then challenged with various doses of ACh or muscarinic receptor agonists (oxotremorine or carbachol) and TRH (100 nM) for 20 min. Significant ACh (10^–5M) suppression of both basal and TRH-induced PRL secretion was not evident in diluent-, E₂- or T₃-pretreated cells, but observed only in cells pretreated with both E₂ and T₃. Moreover, in E₂ plus T₃-pretreated cells, oxotremorine and carbachol, like ACh (10^–7–10^–5M), suppressed both responses in a dose- related manner. Pertussis toxin (PTX; 100 ng/ml) as well as atropine (a muscarinic receptor antagonist; 1 mM) blocked these effects of cholinomimetics. ACh also inhibited both PRL responses elicited by drugs elevating intracellular cAMP (10 µM forskolin) or Ca²⁺ (1 µM Bay K-8644) in a PTX-sensitive manner. ACh inhibition of basal PRL secretion was unaltered by intracellular Ca²⁺ mobilization blockers, TMB-8 (100 µM) and thapsigargin (1 µM), but abrogated by the nitric oxide synthase inhibitor (300 µM L-NAME). ACh inhibition of TRH-induced PRL secretion was accentuated by TMB-8 and alleviated by thapsigargin or L-NAME. In summary, muscarinic inhibition of either basal or TRH-induced PRL secretion was augmented by E₂ and T₃, and involved the PTX-sensitive cAMP/Ca²⁺ pathways. Furthermore, nitric oxide mediated the basal rather than TRH-induced PRL response to ACh, whereas the intracellular Ca²⁺ mobilization concerned the TRH-induced rather than the basal PRL response to ACh. Thus, ACh synthesized in the AP appears to inhibit basal vs. TRH-induced PRL secretion via different mechanisms.

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“…The sensitivity of the assay was 30 pg/tube/ml assay volume. The intra- and interassay coefficients of variation were 9.0 and 14.5%, respectively [27]. …”

Section: Methodsmentioning

confidence: 99%

“…Multiple comparisons were performed where one-way ANOVA was significant, using the Fisher’s least significant difference (LSD) test [28]. Data were subjected to logarithmic transformation before statistical analysis due to heterogeneity of error [27]. All data were expressed as mean ± SEM.…”

Section: Methodsmentioning

confidence: 99%

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Pu¹,

Tan²,

Chen³

et al. 1999

Neuroendocrinology

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Differential involvement of protein kinase C in basal versus acetylcholine‐regulated prolactin secretion in rat anterior pituitary cells during aging

Pu¹,

Liu²

2002

J of Cellular Biochemistry

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Although it is well known that plasma concentration of prolactin (PRL) increases during aging in rats, how the anterior pituitary (AP) aging per se affects PRL secretion remains obscure. The objectives of this study were to determine if changes in the pituitary PRL responsiveness to acetylcholine (ACh; a paracrine factor in the AP), as compared with that to other PRL stimulators or inhibitors, contribute to the known age-related increase in PRL secretion, and if protein kinase C (PKC) is involved. We also determined if replenishment with aging-declined hormones such as estrogen/thyroid hormone influences the aging-caused effects on pituitary PRL responses. AP cells were prepared from old (23-24-month-old) as well as young (2-3-month-old) ovariectomized rats. Cells were pretreated for 5 days with diluent or 17beta-estradiol (E(2); 0.6 nM) in combination with or without triiodothyronine (T(3); 10 nM). Then, cells were incubated for 20 min with thyrotropin-releasing hormone (TRH; 100 nM), angiotensin II (AII; 0.2-20 nM), vasoactive intestinal peptide (VIP; 10(-9)-10(-5) M), dopamine (DA; 10(-9)-10(-5) M), or ACh (10(-7)-10(-3) M). Cells were also challenged with ACh, TRH, or phorbol 12-myristate 13-acetate (PMA; 10(-6) M) following PKC depletion by prolonged PMA (10(-6) M for 24 h) pretreatment. We found that estrogen priming of AP cells could reverse the aging-caused effects on pituitary PRL responses to AII and DA. In hormone-replenished cells aging enhanced the stimulation of PRL secretion by TRH and PMA, but not by AII and VIP. Aging also reduced the responsiveness of cells to ACh and DA in suppressing basal PRL secretion, and attenuated ACh inhibition of TRH-induced PRL secretion. Furthermore, ACh suppressed TRH-induced PRL secretion mainly via the PMA-sensitive PKC in the old AP cells, but via additional mechanisms in young AP cells. On the contrary, basal PRL secretion was PKC (PMA-sensitive)-independent in the old AP cells, but dependent in the young AP cells. Taken together, these results suggest differential roles of PMA-sensitive PKC in regulating basal and ACh-regulated PRL responses in old versus young AP cells. The persistent aging-induced differences in AP cell responsiveness to ACh, DA, TRH, and PMA following hormone (E(2)/T(3)) replenishment suggest an intrinsic pituitary change that may contribute, in part, to the elevated in vivo PRL secretion observed in aged rats.

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Effects of TGF‐β1 on Prolactin Synthesis and Secretion: an In‐Vitro Study

Coya

Álvarez

Franco

et al. 1999

J Neuroendocrinology

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The hypothalamus exerts a predominantly inhibitory influence on prolactin secretion through dopamine. In addition, the expression of anterior pituitary hormone-gene products are regulated by intrapituitary growth factors. In particular, TGF-beta1 produced in the pituitary regulates lactotroph cell proliferation and prolactin gene-expression. This study characterized the regulation of in-vitro prolactin synthesis and secretion by TGF-beta1 using rat anterior pituitary cells in monolayer culture. Furthermore, we studied the interaction of TGF-beta1 with other signals involved in the neuroregulation of prolactin secretion, such as dopamine and TRH, as well as the importance of different signal transduction pathways in this response. TGF-beta1 inhibited prolactin secretion in a time- and concentration-dependent manner, with half-maximal inhibition occurring at the range of 15-30 pM. The inhibitory effect was observed after 4 h, being maximal after 4 days of exposure of the cells to the peptide. This inhibitory effect was mimicked by TGF-beta2 but not by inhibin, and was not influenced by oestrogens, being similar in male, normal female or oestradiol-treated rats. Prolonged pretreatment of the cells with TGF-beta1(4 days) did not modify GH or TSH secretion nor dopamine-induced inhibition of prolactin secretion, and blunted prolactin responses to TRH, Forskolin, But2-cAMP and to the calcium ionophore A23187. The effect observed after long-term treatment (24 h to 4 days) is essentially caused by a decrease in prolactin synthesis, since TGF-beta1 inhibited prolactin mRNA levels and de novo prolactin protein synthesis. However, in the short term (up to 12 h) TGF-beta1 inhibition of prolactin secretion was associated with an increase in intracellular prolactin content, dissecting a dual mechanism of action of TGF-beta1. The short-term TGF-beta1 effect did not modify Erk-2 phosphorylation, basal or TRH-induced increase in intracellular calcium concentration, but blunted basal and forskolin stimulated cAMP levels. But2-cAMP replacement did not revert the inhibition of prolactin secretion. However, pertussis toxin was able to recover a large percentage of TGF-beta1-induced inhibition of prolactin secretion. This study indicates that TGF-beta1 plays a crucial role as a modulator of lactotroph function, inhibiting prolactin biosynthesis after long-term treatment, as well as, after short-term exposure prolactin secretion at the level of the secretory process, through a mechanism pertussis toxin sensitive but independent of Erk-2 phosphorylation, calcium concentrations or intracellular cAMP.

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Differential Effect of Age on Transforming Growth Factor-β1 Inhibition of Prolactin Gene ExpressionVersusSecretion in Rat Anterior Pituitary Cells¹

Cited by 11 publications

References 51 publications

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Differential involvement of protein kinase C in basal versus acetylcholine‐regulated prolactin secretion in rat anterior pituitary cells during aging

Effects of TGF‐β1 on Prolactin Synthesis and Secretion: an In‐Vitro Study

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Differential Effect of Age on Transforming Growth Factor-β1 Inhibition of Prolactin Gene ExpressionVersusSecretion in Rat Anterior Pituitary Cells1

Cited by 11 publications

References 51 publications

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Differential involvement of protein kinase C in basal versus acetylcholine‐regulated prolactin secretion in rat anterior pituitary cells during aging

Effects of TGF‐β1 on Prolactin Synthesis and Secretion: an In‐Vitro Study

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Differential Effect of Age on Transforming Growth Factor-β1 Inhibition of Prolactin Gene ExpressionVersusSecretion in Rat Anterior Pituitary Cells¹