Proliferation and differentiation of pituitary somatotrophs and mammotrophs during late fetal and postnatal periods

Taniguchi, Y.; Yasutaka, Satoru; Kominami, Rieko; Shinohara, Harumichi

doi:10.1007/s429-001-8003-x

Cited by 38 publications

(31 citation statements)

References 25 publications

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“…In this study, the percentage of BrdU-labeled cells was high at day 5 and decreased; however, PRL cells increased in number with age, suggesting that PRL is not synthesized during mitosis of progenitor cells, and differentiated cells begin to produce PRL from days 15 to 20. A similar phenomenon is also reported in rat anterior pituitaries (Taniguchi et al 2001). However, BrdU-and PRL-labeled cells were also found during neonatal period, indicating that some differentiated PRL cells have the potential to proliferate.…”

Section: Discussionsupporting

confidence: 84%

“…Thus, some of the anterior pituitary cells in immature IGF1KO mice may not be able to differentiate into PRL cells in both sexes. PRL cells in the anterior pituitary proliferate and differentiate from late fetal ages to postnatal periods (Taniguchi et al 2001). In this study, the percentage of BrdU-labeled cells was high at day 5 and decreased; however, PRL cells increased in number with age, suggesting that PRL is not synthesized during mitosis of progenitor cells, and differentiated cells begin to produce PRL from days 15 to 20.…”

Section: Discussionmentioning

confidence: 47%

“…5 (Watanabe & Haraguchi 1994, Stefaneanu et al 1999. PRL cells are rarely observed in the fetal anterior pituitary (Ogasawara et al 2009), and these cells begin to increase at postnatal day 3 (Taniguchi et al 2001). Several factors involved in PRL cell proliferation and differentiation have been investigated using knockout (KO) techniques.…”

Section: Introductionmentioning

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: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 47%

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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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“…The defect leading to somatotroph hypoplasia is therefore unlikely to reside in the pituitary but rather involves brain regions which regulate somatotroph proliferation, e.g., the hypothalamus. In rats, somatotroph cells are first detected at embryonic day 18.5 and rapidly increase in number during the first 10 days after birth (27). An important stimulator of somatotroph proliferation is GHRH, and the overexpression of GHRH leads to somatotroph hyperplasia, increased growth, and tumorigenesis, whereas inactivating mutations cause somatotroph hypoplasia and dwarfism (4).…”

Section: Discussionmentioning

confidence: 99%

Loss of G_q/11 Family G Proteins in the Nervous System Causes Pituitary Somatotroph Hypoplasia and Dwarfism in Mice

Wettschureck

Moers

Wallenwein

et al. 2005

Molecular and Cellular Biology

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Heterotrimeric G proteins of the G q/11 family transduce signals from a variety of neurotransmitter and hormone receptors and have therefore been implicated in various functions of the nervous system. Using the Cre/loxP system, we generated mice which lack the genes coding for the ␣ subunits of the two main members of the G q/11 family, gnaq and gna11, selectively in neuronal and glial precursor cells. Mice with defective gnaq and gna11 genes were morphologically normal, but they died shortly after birth. Mice carrying a single gna11 allele survived the early postnatal period but died within 3 to 6 weeks as anorectic dwarfs. In these mice, postnatal proliferation of pituitary somatotroph cells was strongly impaired, and plasma growth hormone (GH) levels were reduced to 15%. Hypothalamic levels of GH-releasing hormone (GHRH), an important stimulator of somatotroph proliferation, were strongly decreased, and exogenous administration of GHRH restored normal proliferation. The hypothalamic effects of ghrelin, a regulator of GHRH production and food intake, were reduced in these mice, suggesting that an impairment of ghrelin receptor signaling might contribute to GHRH deficiency and abnormal eating behavior. Taken together, our findings show that G q/11 signaling is required for normal hypothalamic function and that impairment of this signaling pathway causes somatotroph hypoplasia, dwarfism, and anorexia.The G q/11 family of heterotrimeric G proteins mediates the cellular effects of numerous neurotransmitter receptors, e.g., the metabotropic glutamate receptor subtypes 1 and 5, the M 1 muscarinic-acetylcholine receptor, the 5-HT 2 serotonin receptors, or the ␣ 1 adrenergic receptor. G q/11 -coupled receptors are also involved in the signal transduction of several hypothalamic peptide hormone receptors, such as the receptors for thyrotropin-releasing hormone (39), gonadotropin-releasing hormone (13), and prolactin-releasing hormones (3). There is an increasing amount of evidence that the release of hypothalamic hormones themselves is also controlled by G q/11 -coupled receptors. Kisspeptins, for example, have been suggested to control the release of gonadotropin-releasing hormone via the G q/11 -coupled receptor GPR54 (14,20), and the gastrointestinal peptide hormone ghrelin regulates the production of growth hormone-releasing hormone (GHRH) via the hypothalamic growth hormone secretagogue receptor (GHS-R) (12,22). G q/11 family G proteins mediate the activation of ␤ isoforms of phospholipase C, resulting in the activation of protein kinase C and intracellular calcium mobilization (2). The G q/11 family consists of four members, two of which, G q and G 11 , are expressed almost ubiquitously in the central nervous system (26). Genetic inactivation of the gnaq gene, which codes for the ␣ subunit of G q (G␣ q ), leads to a defect in primary hemostasis (16) and cerebellar ataxia (15). In contrast, mice homozygous for a null allele of the gene coding for G␣ 11 , gna11, did not show any phenotypic abnormalities (17). These...

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“…and, finally, mammotrophic cells at day 19.5 p.c. [60][61][62][63][64]. Given the coincidence in time between cytokine expression detected by us and anterior pituitary functional differentiation during development, IL-1b and IL-6 might influence either the latter or hormonal release, as in adults.…”

Section: Could Il-1b and Il-6 Have An Influence On Hormonal Release Amentioning

confidence: 99%

Prenatal expression of interleukin 1β and interleukin 6 in the rat pituitary gland

et al. 2008

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a b s t r a c tIt is known that interleukin 1b (IL-1b) and interleukin 6 (IL-6) are expressed post-natally in normal and tumoral cells in the anterior pituitary, and that they play a role in both the liberation of different hormones and in the growth, proliferation and tumor formation of the pituitary gland. However, their expression and role during embryonic and fetal development remain unknown. We have performed an immunocytochemistry study of prenatal expression and distribution of IL-1b and IL-6 in isolated embryonic rat Rathke's pouch prior to birth, more specifically between 13.5 and 19.5 days p.c. Western-blot analysis carried out on 19.5-day p.c. embryos showed positive immunolabelling for IL-1b and IL-6. These interleukins were initially expressed simultaneously in the rostral and ventral portions of Rathke's pouch in 15.5-day p.c. embryos, and this expression progressed caudodorsally in later developmental stages, extending to most of the hypophysis before birth. The number of cells expressing these interleukins increased throughout this period: 48.22% of anterior pituitary cells expressed IL-6 in 19.5-day embryos, whilst IL-1b was positive in 39.8% of the cells. Moreover, we have demonstrated that some adenohypophyseal cells co-express both interleukins. Such findings represent the first step towards an understanding of the physiological role of these interleukins in anterior pituitary development.

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Proliferation and differentiation of pituitary somatotrophs and mammotrophs during late fetal and postnatal periods

Cited by 38 publications

References 25 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

Loss of G_q/11 Family G Proteins in the Nervous System Causes Pituitary Somatotroph Hypoplasia and Dwarfism in Mice

Prenatal expression of interleukin 1β and interleukin 6 in the rat pituitary gland

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Proliferation and differentiation of pituitary somatotrophs and mammotrophs during late fetal and postnatal periods

Cited by 38 publications

References 25 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

Loss of Gq/11 Family G Proteins in the Nervous System Causes Pituitary Somatotroph Hypoplasia and Dwarfism in Mice

Prenatal expression of interleukin 1β and interleukin 6 in the rat pituitary gland

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Loss of G_q/11 Family G Proteins in the Nervous System Causes Pituitary Somatotroph Hypoplasia and Dwarfism in Mice