Antisera to Vasoactive Intestinal Polypeptide Inhibit Basal Prolactin Release from Dispersed Anterior Pituitary Cells

Hagen, Thad C.; Arnaout, Mohammed A.; Scherzer, W; Martinson, Donald R.; Garthwaite, Thomas L.

doi:10.1159/000124594

Cited by 105 publications

(37 citation statements)

References 18 publications

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“…PAM activity is expressed in all pituitary hormone-producing cells of the AP, a finding consistent with the presence of a multitude of regulatory peptides, many of which are amidated, in the pituitary gland (16,37,38). To investigate whether TRH acts in a paracrine fashion within cultured AP cells, we chose Dis as a highly specific tool to reduce the formation of bioactive TRH, which we previously established to be expressed in this system (11,12,15,16,28).…”

Section: Discussionmentioning

confidence: 77%

Thyrotropin-Releasing Hormone Gene Expression in the Anterior Pituitary. IV. Evidence for Paracrine and Autocrine Regulation

1998

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Disulfiram (Dis), an inhibitor of peptidyl-glycine ␣-amidating monooxygenase, the enzyme responsible for the production of ␣-amidated peptides from their immediate, glycine-extended precursors was used to investigate the paracrine effects of TRH on anterior pituitary (AP) hormone secretion. It reduces the production of TRH without directly affecting the classical pituitary hormones, none of which is amidated.Dis (8 M) decreased the accumulation of TRH accompanied by an equimolar increase in TRH-Gly levels, indicating that pro-TRH biosynthesis persisted. TRH and TSH release into the medium was significantly lowered, whereas other pituitary hormones were unaffected. In contrast, dexamethasone (10 nM), which up-regulates TRH gene expression in this system, increased TRH (ϩ89.5%) and TSH (ϩ61.3%) secretion. The combination of dexamethasone and Dis further diminished the release of TRH (Ϫ73%) and TSH (Ϫ40.3%) observed with Dis alone, indicating that TRH synthesized within the AP regulates TSH secretion.Dis significantly elevated prepro-TRH (25-50) and pro-TRH messenger RNA levels, suggesting that reduced TRH formation leads to increased pro-TRH biosynthesis and that TRH regulates its own secretion. Thus, TRH synthesized by cultured AP cells not only stimulates TSH release through a paracrine effect, but has a negative feedback on its own biosynthesis by an autocrine mechanism. (Endocrinology 139: 3416 -3422, 1998)

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Section: Discussionmentioning

confidence: 77%

Thyrotropin-Releasing Hormone Gene Expression in the Anterior Pituitary. IV. Evidence for Paracrine and Autocrine Regulation

1998

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“…Moreover, it has been demonstrated in vitro that VIP exerts an autocrine or paracrine role on basal PRL release, both in normal anterior pituitary and GH3 cells [1, 2], hypothyroidism [3], dopamine withdrawal [4], and TRH-stimulated PRL release [5]. …”

Section: Introductionmentioning

confidence: 99%

Role of Vasoactive Intestinal Peptide and 5-HT<sub>2</sub> Receptor Subtype in Serotonin Stimulation of Basal and Thyrotropin-Releasing-Hormone- Induced Prolactin Release in vitro from Rat Pituitary Cells

Apfelbaum¹

1998

Neuroendocrinology

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We have previously demonstrated that 5-HT stimulates not only basal but also thyrotropin-releasing-hormone (TRH)-induced prolactin (PRL) release by acting directly at the pituitary gland level. In the present report, the participation of an autoparacrine action of VIP in the stimulatory effects of 5-HT and the involvement of the 5-HT₂ receptor type in mediating serotonin-induced PRL release have been examined. Cultured anterior pituitary cells from ovariectomized adult rats were incubated for 1 h in 1 ml of T₃-supplemented medium with or without the test substances. The results obtained in the presence of T₃ confirm our previous observations, since treatment of the cells with 5-HT caused dose-dependent increases in basal PRL release, with an approximate EC₅₀ of 3.68 × 10^–8 M, and led to a significant potentiation (1.3-fold) of the TRH-induced PRL release. In order to evaluate the possible participation of vasoactive intestinal peptide (VIP) as mediator of the effects of 5-HT on PRL release, cells were incubated in the presence of 5-HT alone (3–1,000 nM) or 100 nM 5-HT plus 30 nM TRH, with or without 200 nM VIP antagonist (VIP-At): [D,4-Cl-Ph⁶,Leu¹⁷]VIP. VIP-At partially inhibited the release of PRL induced by 5-HT, both basal and TRHstimulated release. The stimulatory effect of 5-HT, however, was not eliminated by VIP-At, since the PRL released in response to 5-HT was still over the respective control ones. These results further support the findings suggesting that 5-HT acts directly at pituitary level by stimulating PRL release. Addition of the 5-HT₂ receptor antagonist, ketanserin (1 µM) into the incubation medium resulted in the loss of cellular responsiveness to 5-HT, preventing not only the stimulatory effect of 5-HT on the basal but also on the TRH-induced PRL release. In conclusion, the results further strengthen the possibility that 5-HT increases the basal PRL release and potentiates the stimulatory effect of TRH by acting directly at the level of the lactotropes. These effects are not simply a consequence of autoparacrine action of VIP. In addition, it was shown that ketanserin completely antagonizes PRL response to 5-HT, indicating the involvement of the 5-HT₂ receptor type in mediating PRL release.

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“…The mitogenic activity of IGF-I on mouse mammotrophs might be indirect, since mammotrophs in mouse pituitaries do not express IGFR1 (Honda et al, 1998). In rat pituitaries, IGF-I also stimulated vasoactive intestinal peptide (VIP) gene expression (Lara et al, 1994), which stimulates PRL release (Hagen et al, 1986;Nagy et al, 1988). Therefore, it is possible that VIP might mediate the effects of IGF-I on the mammotrophs.…”

Section: Insulin-like Growth Factor (Igf)mentioning

confidence: 99%

Intrapituitary Regulatory System of Proliferation of Mammotrophs in the Pituitary Gland

Takahashi

2004

Zoological Science

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-Anterior pituitary cells produce growth factors plus cytokines and their receptors. Although some of these pituitary growth factors and cytokines are known to be involved in the control of cell differentiation, proliferation and hormone production in the pituitary gland, their physiological roles remain unknown. Lots of evidence indicates that they are involved in the regulation of prolactin-secreting mammotroph cell proliferation. The regulation of mammotroph functions is a suitable system for understanding the intrapituitary regulatory system operated by growth factors and cytokines, since mammotrophs are the most actively proliferating cells in female pituitary glands. This review discusses the possible intrapituitary regulation of mammotroph differentiation and proliferation in rat and mouse pituitaries.

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Antisera to Vasoactive Intestinal Polypeptide Inhibit Basal Prolactin Release from Dispersed Anterior Pituitary Cells

Cited by 105 publications

References 18 publications

Thyrotropin-Releasing Hormone Gene Expression in the Anterior Pituitary. IV. Evidence for Paracrine and Autocrine Regulation

Thyrotropin-Releasing Hormone Gene Expression in the Anterior Pituitary. IV. Evidence for Paracrine and Autocrine Regulation

Role of Vasoactive Intestinal Peptide and 5-HT<sub>2</sub> Receptor Subtype in Serotonin Stimulation of Basal and Thyrotropin-Releasing-Hormone- Induced Prolactin Release in vitro from Rat Pituitary Cells

Intrapituitary Regulatory System of Proliferation of Mammotrophs in the Pituitary Gland

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