Effects of diethylstilbestrol on the cytogenesis of prolactin cells in the pars distalis of the pituitary gland of the mouse

Matsubara, Maki; Harigaya, Toshio; Nogami, Hisashi

doi:10.1007/s004410100442

Cited by 20 publications

(23 citation statements)

References 37 publications

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“…In the pituitary, it is known that treatment with DES causes pituitary hyperplasia followed by the development of prolactinomas (Walker and Kurth 1993), and DES increased the prolactin (PRL) cell population in rodent pituitaries (Cauwenberge et al 2001;Matsubara et al 2001). However, the precise mechanism of DES effect on pituitary cells remains unclear.…”

Section: Introductionmentioning

confidence: 98%

Diethylstilbestrol increases the density of prolactin cells in male mouse pituitary by inducing proliferation of prolactin cells and transdifferentiation of gonadotropic cells

Shukuwa

Izumi

Hishikawa

et al. 2006

Histochem Cell Biol

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Diethylstilbestrol (DES) has been implicated in mammalian abnormalities. We examined the effects of DES on follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL) cells in the pituitaries of male mice treated with various doses of DES for 20 days. DES reduced the density of FSH and LH cells in a dose-dependent manner, but increased that of PRL cells. When the expression of estrogen receptor (ER) alpha and beta was assessed, an induction of ERbeta by DES was found predominantly in PRL cells. However, since these effects were abolished in ERalpha knockout mice, DES appears to act primarily through ERalpha. When the expression of Ki-67 and Pit-1 in PRL cells was examined at various time-points after DES treatment, some PRL cells became Ki-67 positive at 10-15 days, and Pit-1-positive cells were increased at 5-15 days. Furthermore, some FSH and LH cells became Pit-1 positive, and co-localized with PRL at 5-10 days. Our results indicate that DES increases PRL cells by inducing proliferation of PRL cells and transdifferentiation of FSH/LH cells to PRL cells.

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Section: Introductionmentioning

confidence: 98%

Diethylstilbestrol increases the density of prolactin cells in male mouse pituitary by inducing proliferation of prolactin cells and transdifferentiation of gonadotropic cells

Shukuwa

Izumi

Hishikawa

et al. 2006

Histochem Cell Biol

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“…These cells are considered to arise from a common precursor cell, and the sequential expression of transcription factors involved in pituitary organogenesis induces differentiation into different endocrine cells. Pituitary endocrine cell development and the specific production of these transcription factors may be controlled by some extracellular signaling molecules, such as fibroblast growth factor 8, bone morphogenetic protein 4 and Wnt5a (Treier et al 1988, Sheng & Westphal 1999, Dasen & Rosenfeld 2001, and steroid hormones (Nogami et al 1995, Stahl et al 1999, Matsubara et al 2001. In addition, the potent ability of cytokines such as leukemia inhibitory factor (Akita et al 1997) might be considered to be essential for pituitary development.…”

Section: Introductionmentioning

confidence: 99%

Multistep differentiation of GH-producing cells from their immature cells

Mogi

Goda

Mogi

et al. 2005

Journal of Endocrinology

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In order to study GH cell differentiation, we used the clonal cell lines called MtT/E and MtT/S cells, which were derived from a rat mammotrophic pituitary tumor. Although MtT/E cells are non-hormone-producing ones, Pit-1 protein is present in their nuclei, which suggests that MtT/E cells are progenitor cells of the Pit-1 cell lineage and have the potential to differentiate into hormoneproducing cells. On the other hand, MtT/S cells produce GH; however, the responsiveness to GH-releasing hormone (GHRH) is weak and only a small number of secretory granules are present in their cytoplasm, which suggests that MtT/S cells are premature GH cells. In order to differentiate into GH cells from MtT/E cells as a progenitor cell, we examined several differentiation factors and found that retinoic acid (RA) induced the differentiation of MtT/E cells into GH-producing cells. RAinduced GH cells partially matured with the glucocorticoid treatment; however, the responsiveness to GHRH on GH secretion was incomplete. In order to elucidate the mechanism underlying full differentiation of GH cells, we used MtT/S cells. We treated MtT/S cells with glucocorticoid and found that they differentiated into mature GH cells with many secretory granules in their cytoplasm and they responded well to GHRH. These results suggested that MtT/E and MtT/S cells are progenitor or premature GH cells, and show different responses to differentiation factors. Our data also suggested that GH cells differentiate from their progenitor cells through multistep processes.

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“…It is well known that long-term E 2 treatment induces mammotrophic pituitary tumors [22,23]. Moreover, diethylstilbestrol could induce PRL cell differentiation in the fetal mouse pituitary [24], and promote PRL cell proliferation in the adult pituitary [25,26]. In this study, we assessed the effect of co-treatment with E 2 and corticosterone on MtT/SM cells, and found that co-treatment with E 2 and corticosterone (10 -12 -10 -9 M) had an additive effect on the induction of PRL-immunopositive cells.…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent Effects of a Glucocorticoid on Prolactin Production

et al. 2008

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Abstract. Glucocorticoids are known to stimulate growth hormone (GH) production but to suppress prolactin (PRL) production. However, previous data were obtained with rather high doses of corticosterone. In this study we examined the effects of various doses (10 -12 -10 -7 M) of corticosterone on GH and PRL production in a rat pituitary somatomammotropic cell line, MtT/SM cells, and found that GH mRNA expression was facilitated by high doses (10 -7 and 10 -8 M). In contrast, a biphasic effect of corticosterone on PRL mRNA expression and secretion was observed, i.e., high doses (10 -7 and 10 -8 M) suppressed and low doses (10 -12 -10 -10 M) facilitated them. In an immunofluorescent staining study, the number of PRL immunopositive cells increased with low doses of corticosterone while it decreased with high doses of it, which corresponded to PRL mRNA expression and hormone secretion, respectively. These effects of corticosterone on PRL production were abolished by a glucocorticoid receptor (GR) antagonist, mifepristone. In addition, co-treatment with low doses of corticosterone (10 -12 -10 -10 M) and 17β-estradiol (E 2 , 10 nM) additively increased the number of PRL immunopositive cells. Moreover, a 24 h BrdU incorporation experiment suggested that the increase in the number of PRL immunopositive cells treated with low dose corticosterone was caused by novel synthesis of PRL while, on the other hand, that of those treated with E 2 resulted from PRL cell proliferation. Thus, we concluded that corticosterone biphasically regulates PRL production and the sensitivity of E 2 to different degrees.

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Effects of diethylstilbestrol on the cytogenesis of prolactin cells in the pars distalis of the pituitary gland of the mouse

Cited by 20 publications

References 37 publications

Diethylstilbestrol increases the density of prolactin cells in male mouse pituitary by inducing proliferation of prolactin cells and transdifferentiation of gonadotropic cells

Diethylstilbestrol increases the density of prolactin cells in male mouse pituitary by inducing proliferation of prolactin cells and transdifferentiation of gonadotropic cells

Multistep differentiation of GH-producing cells from their immature cells

Dose-dependent Effects of a Glucocorticoid on Prolactin Production

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