Relationships between Thyroid Hormone and Glucocorticoid Effects in GH3 Pituitary Cells*

Perrone, Mark H.; Greer, Thomas L.; Hinkle, Patricia M.

doi:10.1210/endo-106-2-600

Cited by 32 publications

(7 citation statements)

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“…in each measurement a control sample containing a known amount of the mRNA under investigation. It should be noted that in previous similar investigations of hormonal regulation of GH synthesis in GH-cells (6, 7, 9, 10, 26), T3 alone stimulated GH synthesis; glucocorticoids alone yielded a moderate (2-to 3-fold) increase in GH synthesis detectable only after 48 hr of incubation, either in medium containing 10% hypothyroid, hyposteroid serum or in serum-free medium (26); and both hormones together yielded a large "synergistic" stimulation of GH synthesis (6,7,9,10,26). In the present experiments, in which GH3 cells were incubated with T3 or dexamethasone or both for 72 hr, we also observed that T3 alone stimulates GH synthesis.…”

Section: Resultsmentioning

confidence: 80%

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Thyroid or glucocorticoid hormone induces pre-growth-hormone mRNA and its probable nuclear precursor in rat pituitary cells.

Dobner¹,

Kawasaki²,

Yu³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

211

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Thyroid or glucocorticoid hormone increases the synthesis of growth hormone (GH) by clonal lines of rat pituitary tumor cells. To investigate whether these increases arise from increased accumulation of GH-specific RNA sequences in the cytoplasm and nuclei of these cells, we adapted two existing procedures so that a 32P-labeled hybrid plasmid containing a cDNA sequence could be used to quantitate relative concentrations ofthe corresponding mRNA. One method (RNA gel blot hybridization) used electrophoresis of RNA, transfer to nitrocellulose paper, and hybridization to 32P-labeled plasmid. The other (RNA dot hybridization) used covalent attachment of RNA to activated cellulose paper squares and hybridization to 32P-labeled plasmid. As probe, we used a hybrid plasmid (pBR322-GHl) which we show by restriction analysis to contain a DNA sequence coding for rat GH. The results were comparable from both techniques and showed that incubation of GH3 cells with a thyroid hormone (triiodothyronine), a glucocorticoid hormone (dexamethasone), or both hormones caused an increase of cytoplasmic pre-GH mRNA sequences of about 4-, 22-, and 13-fold, respectively. Results obtained with the RNA gel blot hybridization method showed that hormonal stimulation leads to the induction of a single 1.0-kilobase species of pre-GH mRNA in the cytoplasm and of 2.7-and 1.0-kilobase species of GH-specific RNA in the nucleus.GH-cells are related lines of rat pituitary tumor cells that produce the protein hormones growth hormone (GH) and prolactin (1,2). Glucocorticoids increase GH production by . The use of hypothyroid serum in the growth medium later led to the demonstration that thyroid hormones also increase GH production by these cells (4). Since then, GH-cells have been used extensively to study the mechanisms of action of glucocorticoid and thyroid hormones (5-7).Recent experiments using in vitro mRNA translation systems have shown that increases in GH synthesis in response to these hormones are accompanied by increases in translatable cytoplasmic pre-GH (pGH) mRNA (8-11). However, the intracellular events leading to increased GH synthesis by GH-cells upon exposure to a glucocorticoid or a thyroid hormone remain unclear. For example, it is not known whether the hormoneinduced increases in translatable cytoplasmic pGH mRNA arise from an increase in cytoplasmic pGH mRNA sequences or from some cellular alteration in the structure of pGH mRNA that increases its translational efficiency. Furthermore, the recent demonstration of a probable nuclear precursor of pGH mRNA (12) raises the possibility that hormone action on GH-cells could be exerted at the level of processing of this precursor into mature cytoplasmic pGH mRNA.To investigate these questions, we have adapted the gel blot hybridization technique of Thomas (13) and the dot hybridization procedure of Kafatos et al. (14) so that a 32P-labeled GH cDNA plasmid [pBR322-GH1 (15)] can be used as probe to detect and quantitate GH-specific RNA sequences. We report here that exposure of G...

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Section: Resultsmentioning

confidence: 80%

“…The use of hypothyroid serum in the growth medium later led to the demonstration that thyroid hormones also increase GH production by these cells (4). Since then, GH-cells have been used extensively to study the mechanisms of action of glucocorticoid and thyroid hormones (5)(6)(7).…”

mentioning

confidence: 99%

Thyroid or glucocorticoid hormone induces pre-growth-hormone mRNA and its probable nuclear precursor in rat pituitary cells.

Dobner¹,

Kawasaki²,

Yu³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

211

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“…Although it has been reported that glucocorticoids decrease PRL synthesis in vitro (Perrone et al 1980), it is still unclear whether glucocorticoids directly affect PRL secretion in the pituitary. Since we confirmed that GR immunoreactivity was not observed in PRL cells, it is probable The present study is the first to demonstrate that other GR-immunopositive cells in the pituitary gland show immunoreactivity for S100 protein.…”

Section: Discussionmentioning

confidence: 99%

Cellular localization and distribution of glucocorticoid receptor immunoreactivity and the expression of glucocorticoid receptor messenger RNA in rat pituitary gland

Ozawa

Itō

Ochiai

et al. 1999

Cell and Tissue Research

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By means of double immunohistochemical techniques and a nonradioisotopic in situ hybridization method, we determined the colocalization pattern of glucocorticoid receptor (GR) and pituitary hormones and the GR messenger RNA (mRNA) expression in the pituitaries of Wistar adult male rats. Immunoreactivity for GR was detected in the nuclei of cells in the anterior and posterior pituitary. Double immunohistochemistry revealed that the colocalization of GR and anterior pituitary hormones occurred in almost 99% of the growth hormone (GH)-producing cells and adrenocorticotropic hormone (ACTH)-producing cells, and in 67% of the thyroid stimulating hormone (TSH)-producing cells. Almost all of the folliculostellate cells (93%), marginal layer cells (94%) in the anterior pituitary, and pituicytes (96%) in the posterior pituitary immunostained for S100 protein antibody were also immunostained with GR. GR mRNA was abundant in the cytoplasm of anterior and intermediate pituitary cells but scattered sparsely in that of the posterior pituitary. These results suggest that glucocorticoids directly influence certain pituitary cells in order to regulate cell function, including the synthesis and/or secretion of hormones.

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“…In addition to the ER, the other members of the superfamily of nuclear receptors (Hurd & Moudgil 1998) known to exist within the GH 3 cells are the progesterone receptor (Newton et al 1994a), the glucocorticoid receptor (Perrone et al 1980), the thyroid hormone receptor and the retinoic acid receptors (Morita et al 1990). Studies over the past decade have demonstrated marked functional crosstalk between receptor systems (Bunone et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone blocks antioestrogen- and oxidant-induced death of pituitary tumour cells

Newton¹,

bilko²,

Pappa³

et al. 2001

Journal of Endocrinology

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The oestrogen receptor is fundamental to the growth and survival of the rat pituitary tumour cell line, GH 3 . Our previous studies have shown that antioestrogens such as RU 58668 and ZM 182780 will reduce the rate of cell division and also induce cell death. Death of these cells in response to antioestrogen treatment appears to be due to a heightened sensitivity to reactive oxygen species (ROS). As part of a study to determine the cross-talk between steroid receptor systems in these cells, we have observed that the glucocorticoid, dexamethasone (Dex), inhibits antioestrogen-induced cell death. Cell death induced by H 2 O 2 is enhanced by ZM 182780 and this effect is also blocked by Dex. As apoptotic cell death in a number of systems involves an early loss of mitochondrial membrane potential ( m ), we have performed detailed studies on the time-course of m loss in relation to the loss in cell membrane function. These studies have indicated that a loss of m parallels a loss of cell membrane functionthis is more characteristic of necrosis than of apoptosis.From microscopic observations of these cells in response to H 2 O 2 , it has been noted that early cell membrane blebbing, induced by H 2 O 2 , is blocked in the presence of ZM 182780. Cell membrane blebbing can precede necrosis as well as apoptosis and it is thought to involve cytoskeletal changes, for which localised glycolytic reactions provide ATP. These observations, together with those showing that removal of glucose, but not inhibition of mitochondrial function, enhances ROS-induced cell death, prompted studies on the glycolytic pathway. As a strong candidate mechanism, it would appear that, via an effect on one of the rate-limiting glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase, Dex is able to overcome the antioestrogen-enhanced loss of glycolytic function following exposure of cells to ROS. This report contributes to the growing body of evidence showing that glucocorticoids provide a survival advantage to both normal and tumour cell types.

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Relationships between Thyroid Hormone and Glucocorticoid Effects in GH3 Pituitary Cells*

Cited by 32 publications

References 0 publications

Thyroid or glucocorticoid hormone induces pre-growth-hormone mRNA and its probable nuclear precursor in rat pituitary cells.

Thyroid or glucocorticoid hormone induces pre-growth-hormone mRNA and its probable nuclear precursor in rat pituitary cells.

Cellular localization and distribution of glucocorticoid receptor immunoreactivity and the expression of glucocorticoid receptor messenger RNA in rat pituitary gland

Dexamethasone blocks antioestrogen- and oxidant-induced death of pituitary tumour cells

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