Antagonic effects of oestradiol in interaction with IGF-1 on proliferation of lactotroph cells in vitro

Gutiérrez, Silvina; Petiti, Juan Pablo; Paul, Ana Lucía De; Mukdsi, Jorge Humberto; Aoki, Agustı́n; Torres, Alicia Inés; Orgnero, Elsa Margarita

doi:10.1007/s00418-005-0038-4

Cited by 18 publications

(20 citation statements)

References 48 publications

(40 reference statements)

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“…Several reports show that E 2 inhibits IGF1 action which induces proliferation of PRL cells in primary culture of rat pituitary (Kawashima et al 2002, Gutiérrez et al 2005. However, an antagonistic effect of estrogen was not observed in this study, it may be due to the use of pituitaries from the developmental period of mice.…”

Section: Discussioncontrasting

confidence: 69%

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

Hikake¹,

Hayashi²,

Iguchi³

et al. 2009

Journal of Endocrinology

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IGF1 knockout (IGF1KO) mice show a reduced number of prolactin (PRL) producing cells (PRL cells); however, the role of IGF1 in PRL cell proliferation and differentiation in immature mice is unclear. In this study, ontogenic changes in the percentages of PRL cells, GH producing cells (GH cells), and 5-bromo-2 0 -deoxyuridine (BrdU)-labeled cells in the anterior pituitary of male IGF1KO mice during the postnatal period were investigated. The percentage of PRL cells in IGF1KO mice was significantly lower at day 20 compared with that in wild-type (WT) mice, while GH cells in IGF1KO mice were significantly increased from day 10. From days 5 to 20, the percentage of BrdU-labeled cells in WT and IGF1KO mice was similar. PRL cells and GH cells are thought to originate from the same progenitor cells, therefore, PRL cells in IGF1KO mice are not able to differentiate because progenitor cells have already committed to be GH cells. However, IGF1, 17b-estradiol (E 2 ), epidermal growth factor (EGF), or IGF1 plus E 2 treatments increased the PRL cell number in the pituitaries in vitro of 10-day-old WT and IGF1KO mice. This fact suggests that these factors are involved in PRL cell proliferation and differentiation. In addition, the increase of PRL cells in IGF1KO mice stimulated by E 2 or EGF was less than that of WT mice. Thus, IGF1 plays a crucial role in PRL cell proliferation and differentiation in mouse pituitaries by regulating the differentiation of progenitor cells and mediating the actions of E 2 and EGF.

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Section: Discussioncontrasting

confidence: 69%

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

Hikake¹,

Hayashi²,

Iguchi³

et al. 2009

Journal of Endocrinology

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“…Although estrogens are associated with proliferative actions on lactotrophs, E2 can also exert antiproliferative effects. Indeed, it has been reported that incubation of anterior pituitary cells with E2 for up to 72 h reduces the mitogenic action of insulin and IGF-1 on lactotrophs [25, 26]. Other findings suggest that the proliferative effect of estrogens on lactotrophs could be mediated by paracrine factors [27].…”

Section: Discussionmentioning

confidence: 99%

Apoptosis of Lactotrophs Induced by D2 Receptor Activation Is Estrogen Dependent

Radl

Zárate²,

Jaita³

et al. 2008

Neuroendocrinology

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Background/Aims: Dopamine (DA) inhibits prolactin release and reduces lactotroph proliferation by activating D2 receptors. DA and its metabolite, 6-hydroxydopamine (6-OHDA), induce apoptosis in different cell types. DA receptors and DA transporter (DAT) were implicated in this action. Considering that estradiol sensitizes anterior pituitary cells to proapoptotic stimuli, we investigated the effect of estradiol on the apoptotic action of DA and 6-OHDA in anterior pituitary cells, and the involvement of the D2 receptor and DAT in the proapoptotic effect of DA. Methods: Viability of cultured anterior pituitary cells from ovariectomized rats was determined by MTS assay. Apoptosis was evaluated by Annexin-V/flow cytometry and TUNEL. Lactotrophs were identified by immunocytochemistry. Results: DA induced apoptosis of lactotrophs in an estrogen-dependent manner. In contrast, estradiol was not required to trigger the apoptotic action of 6-OHDA. Cabergoline, a D2 receptor agonist, induced lactotroph apoptosis, while sulpiride, a D2 receptor antagonist, blocked DA-induced cell death. The blockade of DAT by GBR12909 did not affect the apoptotic action of DA, but inhibited 6-OHDA-induced apoptosis. Conclusion: These data show that DA, through D2 receptor activation, induces apoptosis of estrogen-sensitized anterior pituitary cells, and suggest that DA contributes to the control of lactotroph number not only by inhibiting proliferation but also by inducing apoptosis.

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“…The well-established mitogenic action of E 2 occurs only with long incubation periods and requires the synthesis of local mediators whereas E 2 antimitogenic action has a short latency and needs the presence of growth factors [68]. It has been suggested that E 2 acts selectively in signaling pathways of growth factors to counteract their mitogenic action [69]. Also, the early mitogenic activity promoted by insulin on lactotropes is blocked by E 2 or E 2 -BSA, an action involving PKC, ERK1/2, Pit-1 and probably mERα [30].…”

Section: Mechanisms Of Estrogen Actionmentioning

confidence: 99%

Estrogen Receptors and Signaling Pathways in Lactotropes and Somatotropes

Zárate

Seilicovich²

2010

Neuroendocrinology

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Estrogens are crucial determinants in the regulation of anterior pituitary function and maintenance of tissue homeostasis. Estrogen actions in this gland are exerted through both classical and non-classical mechanisms of action. This review summarizes the expression of classical α- and β-estrogen receptors and variant isoforms of estrogen receptors in anterior pituitary cell subpopulations. We also analyze estrogen receptor signaling pathways involved in estrogenic actions in the anterior pituitary gland, especially in lactotropes and somatotropes. Complex interactions between multiple signaling pathways are involved in estrogen regulation of hormone secretion, cell proliferation and cell death in this gland. Insight into these pituitary responses to estrogens would help to understand pituitary function and tumorigenesis.

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Antagonic effects of oestradiol in interaction with IGF-1 on proliferation of lactotroph cells in vitro

Cited by 18 publications

References 48 publications

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

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

Apoptosis of Lactotrophs Induced by D2 Receptor Activation Is Estrogen Dependent

Estrogen Receptors and Signaling Pathways in Lactotropes and Somatotropes

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