Prolactin-Producing Cells Differentiate from G0/G1-Arrested Somatotrophs In Vitro: An Analysis of Cell Cycle Phases and Mammotroph Differentiation.

Goda, Hideki; Sakai, Takafumi; Kurosumi, Masafumi; Inoue, Kinji

doi:10.1507/endocrj.45.725

Cited by 16 publications

(13 citation statements)

References 20 publications

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“…Furthermore, EGF plays a role in cell proliferation and differentiation in the mouse anterior pituitary (Schwardz 2000). EGF induces the expression of dopamine receptor and transdifferentiation into lactotroph-like cells in the GH3 cell line (Missale et al 1991) and PRL cell differentiation in the MtT/S cell line (Goda et al 1998). Ben-Jonathan et al (2009) show that the ability of EGF to stimulate Prl gene expression and release is mediated by Erk1/2-induced phosphorylation of Esr1 in GH3 cells, which express both Esr1 and Esr2 (Mitchner et al 1999).…”

Section: Discussionmentioning

confidence: 98%

“…Several factors may be related to PRL cell proliferation and/or differentiation, including E 2 , IGF1, and EGF. E 2 stimulates PRL cell proliferation (Wiklund et al 1981, Amara et al 1987) and E 2 also induces transdifferentiation of PRL cells from GH cells via somatolactotrophs (Behringer et al 1988, Borrelli et al 1989, Goda et al 1998. Furthermore, EGF plays a role in cell proliferation and differentiation in the mouse anterior pituitary (Schwardz 2000).…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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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“…In contrast, MtT/S cells are GH-producing ones and their character as endocrine cells has been well studied (Goda et al 1998, Nogami et al 2000. MtT/S cells produce GH in normal medium; however, the responsiveness to GH-releasing hormone (GHRH) is weak and only a few secretory granules are present in their cytoplasm, which suggests that MtT/S cells are premature GH ones.…”

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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“…Examples of endocrine cell transdifferentiation include pituitary (GH to TSH [8,23], GH to PRL [24][25][26][27][28] and GH to gonadotroph cells [29]), thyroid C cells [30] and adrenal chromaffin cells [31,32]. The process of pituitary transdifferentiation [8] implies the existence of bi-hormonal cells as intermediates, it does not require cell division [24,26,27] and can be induced by stimulation of hormonal feedback systems [8,23,28] or by treatment with growth factors [24,27].…”

Section: Discussionmentioning

confidence: 99%

Somatotroph to thyrotroph cell transdifferentiation during experimental hypothyroidism ‐ a light and electron‐microscopy study

Radian

Coculescu

Morris

2003

J Cellular Molecular Medi

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Somatotroph and thyrotroph pituitary cells share a common precursor cell expressing the transcription factor Pit1 in ontogeny. Cells expressing both thyrotropin (TSH) and growth-hormone (GH) are found in adult rat pituitary and in human pituitary adenomas in acromegaly, and these tumors contain both thyrotropin-releasing hormone (TRH) and the TRH receptors (TRHR). It has been shown that stimulation of TSH expression in primary hypothyroidism promotes changes suggestive of somatotroph to thyrotroph cell transdifferentiation. We tested this hypothesis and the role of TRH in experimental primary hypothyroidism in rats. Adult female Long-Evans rats, 6 months old, were administered the antithyroid drug methimazole (0,1% w/v) in the drinking water for 42 days. Animals were sacrificed by perfusion fixation under anaesthesia at weekly intervals and pituitary tissue processed in acrylic resin for immunofluorescence and immuno-electronmicroscopy for TSH, GH and TRHR. In the hypothyroid rat pituitary immunofluorescent somatotrophs were greatly reduced in number and gradually replaced by thyrotrophs during methimazole administration. Colocalization of GH and TSH in the same cell was noted. Immunoelectronmicroscopy demonstrated the development of enlarged thyrotrophs with dilated rough endoplasmic reticulum containing an electron-dense material and intracisternal granules, both of which are immunoreactive for TSH ('thyroidectomy cells'). The somatotrophs showed reduced GH immunoreactivity and also the presence of TSH-type, small-size secretory granules. This suggests that the greatly increased number of TSH-cells in methimazole-induced-hypothyroidism is due, at least partially, to the transdifferentiation of somatotroph into thyrotroph cells. TRHR immunofluorescence was expressed in many somatotrophs in normal rat pituitary and unlike immunoreactive GH, its expression was enhanced during hypothyroidism. The number of TRHR-immunoreactive cells increased in parallel with the number of TSH-immunoreactive cells. This indicates a role for TRH stimulation in the transdifferentiation process. Taken together, these data suggest that, in addition to the cell mutation mechanism involving an early totipotential progenitor cell, transdifferentiation of existing somatotroph cells also plays a part in the pathogenesis of multihormonal GH-secreting adenomas.

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Prolactin-Producing Cells Differentiate from G0/G1-Arrested Somatotrophs In Vitro: An Analysis of Cell Cycle Phases and Mammotroph Differentiation.

Cited by 16 publications

References 20 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

Multistep differentiation of GH-producing cells from their immature cells

Somatotroph to thyrotroph cell transdifferentiation during experimental hypothyroidism ‐ a light and electron‐microscopy study

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