The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary

Hikake, Tamiki; Hayashi, Shinji; Iguchi, Taisen; Satō, Tomomi

doi:10.1677/joe-09-0232

Cited by 20 publications

(14 citation statements)

References 47 publications

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“…These are new findings as hypothalamic IGF-I and IGFBP-3 have not been shown to control prolactin secretion in mothers. Previous studies have revealed that IGF-I acts on lactation at the level of the pituitary by supporting the differentiation and proliferation of lactotroph cells 47, 48 . The involvement of hypothalamic IGF-I in reproductive neuroendocrine functions has been suggested before; it plays a role in the regulation of gonadotropin-releasing hormone (GnRH) cell function.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor I and its binding protein-3 are regulators of lactation and maternal responsiveness

Lékó

Cservenák

Szabó

et al. 2017

Sci Rep

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Adaptation to motherhood includes maternal behaviour and lactation during the postpartum period. The major organizing centres of maternal behaviour and lactation are located in the hypothalamic medial preoptic area (MPOA) and the arcuate nucleus, respectively. Insulin-like growth factor I (IGF-I) is an effector of the growth hormone axis; however, its function in the brain is largely unexplored. We identified increased maternal IGF binding protein-3 (IGFBP-3) expression in preoptic rat microarray data and confirmed it by RT-PCR. In situ hybridization histochemistry showed markedly elevated IGFBP-3 expression in the MPOA and the arcuate nucleus in rat dams. Prolonged intracerebroventricular injection of IGF-I or antagonism of brain IGFBP-3 with an inhibitor (NBI-31772) using osmotic minipumps increased pup retrieval time, suggesting reduced maternal motivation. Suckling-induced prolactin release and pup weight gain were also suppressed by IGF-I, suggesting reduced lactation. In addition, IGF-I-induced tyrosine hydroxylase expression and its specific phosphorylation in tuberoinfundibular dopaminergic neurons suppress prolactin secretion. Thus, IGF-I may inhibit both behavioural and lactational alterations in mothers. Neurons in the MPOA and arcuate nuclei express IGFBP-3 during the postpartum period to neutralize IGF-I effects. IGFBP-3 can prevent the blockade of maternal behaviour and lactation exerted by IGF-I, suggesting a novel modulatory mechanism underlying the behavioural and hormonal effects during central maternal adaptations.

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Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor I and its binding protein-3 are regulators of lactation and maternal responsiveness

Lékó

Cservenák

Szabó

et al. 2017

Sci Rep

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“…At birth only a few cells expressing PRL can be detected but there is a rapid post-natal expansion, increasing in mice exponentially from birth to 5 weeks, before stabilising around 8 weeks of age [54]. The post-natal expansion of lactotrophs is regulated by a number of peripheral, hypothalamic and intrapituitary factors, including insulin-like growth factor 1, epidermal growth factor and estradiol [55]. In the adult, it is clear that dopamine (DA) [25], acting through the dopamine 2 receptor (D2R) is a major suppressor of lactotroph proliferation [56,57], but the increased severity of lactotroph hyperplasia found in Prl −/− or Prlr −/− mice compared with those with a loss of functional DA signalling demonstrates that other factors also regulate lactotroph proliferation [58].…”

Section: Normal Regulation Of Prl Cell Number Gene Expression and Sementioning

confidence: 99%

Plasticity of the Prolactin (PRL) Axis: Mechanisms Underlying Regulation of Output in Female Mice

Tissier

Hodson

Martin

et al. 2014

Advances in Experimental Medicine and Biology

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The output of prolactin (PRL) is highly dynamic with dramatic changes in its secretion from the anterior pituitary gland depending on prevailing physiological status. In adult female mice, there are three distinct phases of output and each of these is related to the functions of PRL at specific stages of reproduction. Recent studies of the changes in the regulation of PRL during its period of maximum output, lactation, have shown alterations at both the level of the anterior pituitary and hypothalamus. The PRL-secreting cells of the anterior pituitary are organised into a homotypic network in virgin animals, facilitating coordinated bouts of activity between interconnected PRL cells. During lactation, coordinated activity increases due to the changes in structural connectivity, and this drives large elevations in PRL secretion. Surprisingly, these changes in connectivity are maintained after weaning, despite reversion of PRL output to that of virgin animals, and result in an augmented output of hormone during a second lactation. At the level of the hypothalamus, tuberoinfundibular dopamine (TIDA) neurons, the major inhibitors of PRL secretion, have unexpectedly been shown to remain responsive to PRL during lactation. However, there is an uncoupling between TIDA neuron firing and dopamine secretion, with a potential switch to enkephalin release. Such a process may reinforce hormone secretion through dual disinhibition and stimulation of PRL cell activity. Thus, integration of signalling along the hypothalamo-pituitary axis is responsible for increased secretory output of PRL cells during lactation, as well as allowing the system to anticipate future demands.

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“…Real-time PCR was carried out with a Smart Cycler® II System with a total reaction volume of 25 μl consisting of 12.5 μl SYBR Green Master Mix (Takara Bio, Otsu, Japan) by the standard curve method. Primer sequences and the details of real-time RT-PCR were as described previously (Hikake et al 2009). Cyclophilin was chosen as an internal standard to control variability in amplification due to differences in starting mRNA concentration.…”

Section: Real-time Rt-pcrmentioning

confidence: 99%

“…The role of IGF-I in the pituitary has been studied in IGF-I KO mice, which carry a disrupted IGF-I gene (Stefaneanu et al 1999;Hikake et al 2009). In adult KO mice, growth hormone (GH) cells are diminished in size but the GH mRNA signal is strong, and the number of PRL cells is decreased.…”

Section: Introductionmentioning

confidence: 99%

Involvement of insulin-like growth factor-I for the regulation of prolactin synthesis by estrogen and postnatal proliferation of lactotrophs in the mouse anterior pituitary

et al. 2010

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Estradiol (E2) stimulates not only secretion of prolactin (PRL) and proliferation of PRL-producing cells (PRL cells) in the anterior pituitary, but also the expression of growth factors. In insulin-like growth factor-I (IGF-I) knockout (KO) mice, the number of PRL cells is decreased and administration of IGF-I does not increase either the number of PRL cells or plasma PRL levels, indicating that IGF-I plays a pivotal role in PRL cells. The effect of E2 on PRL cells in KO mice was investigated by immunohistochemistry and real-time RT-PCR. The number of PRL cells in KO mice was significantly lower than in the wild-type (WT) control mice. E2 increased the PRL mRNA in WT and KO mice; however, an increase of PRL mRNA in KO was less than that in WT. In addition, no vasoactive intestinal peptide (VIP)-immunoreactive cells were found in KO mice, therefore IGF-I is essential for VIP expression. To investigate the roles of IGF-I on PRL cells in the postnatal development, double-immunostaining with PRL and BrdU was performed in WT and KO mice from days 5-20. The percentages of PRL cells and BrdU-labeled cells in the anterior pituitary of KO mice were lower than in WT mice. Thus, IGF-I may be responsible for proliferation and differentiation of PRL cells in this postnatal period. Differentiation and the proliferation of PRL cells are controlled by IGF-I during the postnatal development, and IGF may be a mediator of E2 action through VIP induction in PRL cells of adults.

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The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary

Cited by 20 publications

References 47 publications

Insulin-like growth factor I and its binding protein-3 are regulators of lactation and maternal responsiveness

Insulin-like growth factor I and its binding protein-3 are regulators of lactation and maternal responsiveness

Plasticity of the Prolactin (PRL) Axis: Mechanisms Underlying Regulation of Output in Female Mice

Involvement of insulin-like growth factor-I for the regulation of prolactin synthesis by estrogen and postnatal proliferation of lactotrophs in the mouse anterior pituitary

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