Effects of insulin‐like growth factor‐I on growth hormone and prolactin secretion and cell proliferation of human somatotrophinomas and prolactinomas <i>in vitro</i>

Atkin, Stephen L.; Am, Landolt; P, Foy; Rv, Jeffreys; Hipkin, L. J.; Mc, White

doi:10.1111/j.1365-2265.1994.tb02582.x

Cited by 18 publications

(13 citation statements)

References 23 publications

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“…Although the actions of many of these estrogen-responsive growth regulatory factors have been tested in tumor lactotropes (e.g. GH3 cells) or in mixed pituitary cell populations [52][53][54][55][56][57][58], the actions of most of these factors in primary lactotropes have not been tested or persistent hyperprolactinemia was observed in 16 alcoholic women during a 6-week treatment trial [32]. These patients reported daily alcohol intake of 170 g for a period between 2 and 16 years period but had no clinical evidence of alcoholic liver cirrhosis.…”

Section: Cell Cycle Genomic Instability and Tumorigenesis In Lactotmentioning

confidence: 99%

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Sarkar

2006

Frontiers of Hormone Research

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Prolactin-secreting adenomas (prolactinomas) are the most prevalent form of pituitary tumors in humans. Our knowledge of the formation of these tumors is limited. Experimental work in animal has uncovered that estradiol exposure leads to prolactinoma formation via orchestrated events involving dopamine D2 receptors, transforming growth factor-β (TGF-β) isoforms and their receptors, as well as factors secondary to TGF-β action. Additionally, these studies determined that TGF-β and b-FGF interact to facilitate the communication between lactotropes and folliculo-stellate cells that is necessary for the mitogenic action of estradiol. The downstream signaling that governs lactotropic cell proliferation involves activation of the MAP kinase p44/42-dependent pathway.Pituitary tumors are primarily adenomas; they account for approximately 10-15% of intracranial tumors. They cause significant morbidity due to local invasion, hypopituitarism or hormone hypersecretion [1,2]. Pituitary tumors are classified as either functioning and secreting excessive amounts of active hormones, or as endocrinologically inactive and secreting no hormones or inactive hormones. Pituitary tumors are also classified by virtue of their size into the arbitrary division of those less than 1 cm as microadenomas and those more than 1 cm as macroadenomas. Pituitary tumors secreting excess prolactin are characterized as prolactinomas. Prolactinomas are the most frequently occurring neoplasm in the human pituitary [3,4]. In the general population, 1:2,800 men and 1:1,050 women are considered to have prolactinomas [5]. In human subjects, prolactinomas occur as both macroadenomas and microadenomas. In addition, mixed growth hormone and prolactin-secreting adenomas are documented to exist in a substantial number of acromegaly patients.Hyperprolactinoma is a condition in which plasma prolactin (PRL) levels are elevated above normal levels. Hyperprolactinemia, with elevation of serum prolactin of more than 200 ng/ml, is characteristically associated with prolactinomas [6]. Hyperprolactinemia causes reproductive dysfunction such as amenorrhea, galactorrhea, and infertility in women [7]. Amenorrhea and galactorrhea may occur alone or together [8]. Up to 25% of patients with secondary amenorrhea have been diagnosed with hyperprolactinemia. Many of these patients showed micro-prolactin adenomas or macro-prolactin adenomas in the pituitary. Although treatments that alter central dopaminergic neuronal functions cause an elevated serum PRL level, in most cases hyperprolactinemia is due to a pituitary tumor. In women, prolactinomas are mainly microadenomas. These microadenomas are rarely associated with hypopituitarism or central nervous system dysfunction. Idiopathic hyperprolactinemia, without demonstrable pituitary or hypothalamic disease, has also been identified. In men, prolactinomas are mainly

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Section: Cell Cycle Genomic Instability and Tumorigenesis In Lactotmentioning

confidence: 99%

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Sarkar

2006

Frontiers of Hormone Research

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“…In this study we clearly show that recombinant IGF-I stimulates the release of fractional, total, and newly synthesized PRL from normal cells maintained under completely defined, hormone-free culture conditions. Interestingly, in this latter study a stimulation of PRL release was seen in only those tumors derived from individuals exhibiting low circulating PRL levels and secreting low levels of PRL in vitro (31). It also appears that IGF's stimulatory action on PRL release may be dependent in part on the length of exposure.…”

Section: Discussionmentioning

confidence: 61%

Insulin-Like Growth Factor I Disparately Regulates Prolactin and Growth Hormone Synthesis and Secretion: Studies Using the Teleost Pituitary Model¹

2000

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Although insulin-like growth factor I (IGF-I)'s inhibition of GH release is well documented, little is known of its control of GH synthesis at the posttranscriptional level. The manner by which IGF-I alters PRL synthesis and secretion is also unclear. This study was undertaken to examine the role IGF-I plays in regulating in vitro PRL and GH synthesis and release using the teleost pituitary model system. This model allows for isolation of nearly homogenous populations of distinct pituitary cell types that can be cultured in a completely defined, hormone-free medium. Tissues containing PRL cells and those consisting of GH cells were dissected from pituitaries of hybrid striped bass and exposed to varying concentrations of IGF-I, IGF-II, and insulin for 18-20 h. Exposure to graded doses of IGF-I markedly stimulated fractional, total, and newly synthesized PRL release in a dose-dependent fashion (ED50 for fractional release, 35 ng/ml or 4.6 nM; P < 0.0001). IGF-II and insulin also increased PRL release, but only at 10-fold higher concentrations than the lowest effective IGF-I dose. The total PRL content in the incubations and PRL synthesis, as measured by [35S]methionine incorporation, were not altered by IGF-I. By contrast, IGF-I potently reduced GH release (ED50, 29 ng/ml or 3.8 nM; P < 0.0001) and synthesis. Both 100 and 1000 ng/ml IGF-I decreased newly synthesized GH and total GH content (P < 0.001). Insulin and IGF-II mimicked IGF's action in attenuating GH release, but only at 10- to 11-fold higher concentrations. Taken together, these findings clearly indicate that IGF-I disparately regulates PRL and GH synthesis and secretion. We show that the effects of IGF-I on pituitary hormone release occur in a variety of species, suggesting that its actions are well conserved. The inhibition of GH release and synthesis by IGF-I probably reflects a negative feedback loop for maintaining tight control over GH cell function. These findings further indicate that IGF-I is a potent and specific secretagogue of PRL release in vertebrates.

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“…In rat pituitary monolayer cell cultures, IGF‐I inhibited basal and growth hormone releasing hormone (GHRH)‐stimulated GH secretion and GH mRNA levels ( 22, 23). IGF‐I reduced GH secretion in five out of eight human somatotrophinomas ( 24) and significantly decreased the levels of GH mRNA in rat pitiutary GH3 cells ( 25). In addition to these in‐vitro studies, in‐vivo data in rat show an inverse relationship between circulating IGF‐I concentrations and pituitary GH ( 26, 27).…”

Section: Discussionmentioning

confidence: 99%

“…In human pituitary tumours, evidence has been obtained that IGF‐I may also exert effects on the PRL cells. IGF‐I stimulated PRL release in about 70% of the adenomas over 4 days but inhibited GH release ( 24). In correlation, in the rat pituitary cell line GH4C1, IGF‐I significantly increased PRL mRNA levels ( 25).…”

Section: Discussionmentioning

confidence: 99%

Insulin‐Like Growth Factor I in the Anterior Pituitary of the Clawed Frog Xenopus laevis: Immunocytochemical and Autoradiographic Indication for a Paracrine Action and Corelease with Prolactin

David

Bosshard

Kloas

et al. 2000

J Neuroendocrinology

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Insulin-like growth factor I (IGF-I) and its receptor are present in human and rat anterior pituitary. However, few data exist on the potential presence of IGF-I or its receptor in the non-mammalian pituitary and the cellular sites of IGF-I production have not been identified in any species. Thus, we investigated the anterior pituitary of the clawed frog Xenopus laevis which is widely used to study growth and differentiation. The study was performed with antisera against mammalian insulin-like growth factor I (IGF-I), prolactin (PRL) and growth hormone (GH) using immunohistochemical and immunocytochemical techniques. IGF-I binding was determined by in-vitro receptor autoradiography. The PRL-and GH-immunoreactive cells exhibited distinct distribution patterns. Neither at the light nor the electron microscopical level any colocalization of PRL-and GH-immunoreactivities was apparent. The PRL-immunoreactive cells exhibited round granules of medium electron density (mean diameter: 312 nm) and the GH-immunoreactive cells spherical granules of medium electron density (mean diameter: 165 nm). By the use of serial semithin sections IGF-I-immunoreactivity was exclusively located in PRL-immunoreactive cells. At the ultrastructural level, IGF-I-immunoreactivity was confined to the secretory granules in coexistence with PRL-immunoreactivity using the double labelling immunogold technique. Specific IGF-I binding sites were localized throughout the pituitary. The results provide evidence for a concomitant release of PRL and IGF-I and suggest autocrine/paracrine actions of IGF-I in the anterior pituitary.

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Effects of insulin‐like growth factor‐I on growth hormone and prolactin secretion and cell proliferation of human somatotrophinomas and prolactinomas in vitro

Cited by 18 publications

References 23 publications

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Insulin-Like Growth Factor I Disparately Regulates Prolactin and Growth Hormone Synthesis and Secretion: Studies Using the Teleost Pituitary Model¹

Insulin‐Like Growth Factor I in the Anterior Pituitary of the Clawed Frog Xenopus laevis: Immunocytochemical and Autoradiographic Indication for a Paracrine Action and Corelease with Prolactin

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Effects of insulin‐like growth factor‐I on growth hormone and prolactin secretion and cell proliferation of human somatotrophinomas and prolactinomas in vitro

Cited by 18 publications

References 23 publications

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Insulin-Like Growth Factor I Disparately Regulates Prolactin and Growth Hormone Synthesis and Secretion: Studies Using the Teleost Pituitary Model1

Insulin‐Like Growth Factor I in the Anterior Pituitary of the Clawed Frog Xenopus laevis: Immunocytochemical and Autoradiographic Indication for a Paracrine Action and Corelease with Prolactin

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Insulin-Like Growth Factor I Disparately Regulates Prolactin and Growth Hormone Synthesis and Secretion: Studies Using the Teleost Pituitary Model¹