Rapid stimulation of type I 5′-deiodinase in rat pituitaries by 3,3′,5-triiodo-l-thyronine

Köhrle, Josef; Schomburg, Lutz; Drescher, Simon; Fekete, E.; Bauer, Karl

doi:10.1016/0303-7207(95)92574-8

Cited by 47 publications

(33 citation statements)

References 35 publications

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“…Nevertheless, stimulation of D1 activity in the AP after LPS treatment was very rapid (1 h) and only transient (basal levels were reached after 4 h), suggesting that mechanisms other than transcriptional regulation, e.g. the effects of T 3 on D1 in the AP (Köhrle et al 1995) or new protein synthesis, e.g. the effects of IL-1 , TNF and IL-6 in human liver cells, are responsible for this stimulation.…”

Section: Discussionmentioning

confidence: 97%

“…D2 is involved in thyroid-stimulating hormone (TSH) feedback regulation especially under hypothyroid conditions (Köhrle 1999, Larsen et al 1981. Apart from D2, D1 is also expressed in the anterior pituitary (AP) and may play an important integrative role in the regulation of hormone production and pituitary feedback regulatory mechanisms (Köhrle 1996, 1999, Köhrle et al 1995, Braverman 1994. It is known that D1 is modulated by cytokines but the reports are controversial depending on species, method of cytokine application and organs concerned (Ozawa et al 1988, Pang et al 1989, Tang et al 1995, Pekary et al 1994, Ongphiphadhanakul et al 1994, Davies et al 1997.…”

Section: Introductionmentioning

confidence: 99%

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Effects of proinflammatory cytokines on anterior pituitary 5'-deiodinase type I and type II

Baur¹,

Bauer²,

Jarry³

et al. 2000

Journal of Endocrinology

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Cytokines are locally produced in the anterior pituitary and act through para-/autocrine mechanisms to modulate cell growth and hormone production. 5 -Deiodinases type I (D1) and type II (D2) are also expressed in the anterior pituitary and play an integrative role in the regulation of hormone production and pituitary feedback. D1 activity is known to be regulated by proinflammatory cytokines in liver and thyroid. Therefore, we examined the effects of IL-1 , IL-6 and TNF on 5 -deiodinase activities in reaggregates of rat anterior pituitaries and rat somatomammotroph GH3 cells cultured alone, or in a bicameral culture system together with the murine folliculo-stellate (FS) cell line TtT/Gf. In reaggregate cultures of rat anterior pituitaries IL-1 stimulated D1 and D2 dosedependently and D2 activity was increased by TNF . When GH3 cells were cocultured with TtT/Gf cells, D2 activities were 2·3-fold lower than in GH3 cells cultured alone. TNF (50 ng/ml) and IL-6 (100 U/ml) stimulated D2 in GH3 cells when the cells were cultured alone and treated with these cytokines for 24 h. When TtT/Gf cells in the coculture model were treated with IL-1 , TNF and IL-6, no effect on D1 or D2 activities in GH3 cells was observed.In male, adult rats a single LPS injection (i.p.) stimulated D2 and D1 activities in the anterior pituitary, and decreased liver D1 activities and serum TSH levels. In vitro, LPS stimulation of the coculture model of GH3 and FS cells also increased D1 activity.Electrophoretic mobility shift assays (EMSAs) revealed that IL-1 and TNF activate the transcription factor NF B in reaggregates of rat anterior pituitaries and in TtT/Gf cells cultured alone or cocultured with GH3 cells. Taken together, these findings imply that in anterior pituitary cells 5 -deiodinase activities are stimulated by locally produced cytokines in a para-/autocrine manner but cell types other than FS cells seem to mediate some of the effects.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Effects of proinflammatory cytokines on anterior pituitary 5'-deiodinase type I and type II

Baur¹,

Bauer²,

Jarry³

et al. 2000

Journal of Endocrinology

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“…These data suggest that T 4 , because of its weaker affinity for the receptor, may act after deiodination into T 3 (McNabb 1992). Local deiodination of T 4 into T 3 is regulated by type II and type I 5 -deiodinases in rat anterior pituitary cells (Köhrle et al 1995). Although deiodinase activities have been characterized in various tissues in teleosts, including liver, kidney, gill and brain (Eales et al 1993), the existence of such enzymes in the pituitary has not yet been determined.…”

Section: Discussionmentioning

confidence: 99%

Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

Rousseau¹,

Belle²,

Sbaihi³

et al. 2002

Journal of Endocrinology

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The regulation of growth hormone (GH) by thyroid hormones (THs) has been shown to present species variation. We investigated the regulation of GH in the eel, a representative of an ancient group of teleosts. In vivo administration of triiodothyronine (T 3 ) or thyroxine (T 4 ) significantly reduced pituitary and serum GH levels, as measured by homologous RIA. In order to investigate the ability of THs to regulate GH production directly at the pituitary level, we used a long-term, serum-free primary culture of eel pituitary cells. Both T 3 and T 4 inhibited GH release in a concentration-dependent manner, producing up to 50% inhibition at 10 nM, with an ED 50 of <0·2 nM, within the range of their physiological circulating levels. Other hormones also acting via the nuclear receptor superfamily, such as sex steroids (testosterone, estradiol and progesterone) and corticosteroid (cortisol), had no effect on GH release in vitro, underlining the specificity of the regulatory effect of THs on GH. Measurement of both GH release and cellular content for calculation of GH production in vitro indicated that THs not only inhibited GH release but also GH synthesis. Dot-blot assay of GH messenger RNA (mRNA) using an homologous eel cDNA probe showed a decrease in GH mRNA levels in cells cultured in the presence of T 3 , as compared with control cells. This demonstrated that the inhibition of T 3 on GH synthesis was mediated by a decrease in GH mRNA steady state levels. In conclusion, we demonstrate inhibitory regulation of eel GH synthesis and release by THs, exerted directly at the pituitary level. These data contrast with the rat, where THs are known to have a stimulatory effect and suggest that the pattern observed here in an early vertebrate and also found in birds, reptiles and some mammals including humans, may represent an ancestral and more generalized vertebrate pattern of TH regulation of pituitary GH.

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“…In the pituitary gland of euthyroid rats, half of the T 3 bound to specific nuclear T 3 -receptors (predominantly TR-b2) is derived from local, intrapituitary T 4 -to-T 3 conversion via deiodinase isoenzymes (4). So far, no evidence has been presented for an inactivation pathway of thyroid hormones via the 5-deiodinase (D3) in anterior pituitary models (5). Recently, we demonstrated that D1 is expressed in rat anterior pituitaries, in reaggregates of rat anterior pituitaries, and in rat somatomammotroph GH3 cells.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, we demonstrated that D1 is expressed in rat anterior pituitaries, in reaggregates of rat anterior pituitaries, and in rat somatomammotroph GH3 cells. D1 is stimulated by T 3 and its 5 0 -deiodination product, 3,5-di-iodothyronine (3,5-T 2 ), and may serve a yet unrecognized, important function within the modulation of thyroid-hormone-dependent genes in the anterior pituitary (5,6). Therefore, we have now examined the expression of D1 and its regulation by thyroid hormones in the human somatomammotroph cell line, GX.…”

Section: Introductionmentioning

confidence: 99%

Type 1 deiodinase is stimulated by iodothyronines and involved in thyroid hormone metabolism in human somatomammotroph GX cells

Baur

Köhrle

1999

European Journal of Endocrinology

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Background: Local 5 0 -deiodination of L-thyroxine (T 4 ) to the active thyroid hormone, 3,3 0 ,5-tri-iodothyronine (T 3 ) via two deiodinase isoenzymes (D1 and D2) has an important role for various T 3 -dependent functions in the anterior pituitary. However, no evidence has been presented yet for thyroid hormone inactivation via the 5-deiodinase (D3) in anterior pituitary models. Methods: Using the human somatomammotroph cell line, GX, we analysed effects of T 3 and its 5 0 -deiodination product, 3,5-di-iodothyronine (3,5-T 2 ), on deiodinase activities, measuring release of iodide-125 ( 125 I ¹ ) from phenolic-ring-or tyrosyl-ring-labelled substrates respectively. Results: T 3 and 3,5-T 2 rapidly stimulated D1 activity in GX cells in the presence of serum in the culture medium, whereas D2 activity was not detectable under these conditions. However, when the cells were kept under serum-free conditions, specific activity of D2 reached levels similar to those of D1. With tyrosyl-ring labelled 3,5-[125 I]-,3 0 -T 3 as substrate, a significant release of 125 I ¹ was observed in GX cell homogenates. This is comparable to the D1 activity of liver membranes, which preferentially catalyses 5 0 -deiodination, but to some extent also 5-deiodination, at the tyrosyl ring. Conclusions: D1 activity of human GX cells is increased by T 3 and 3,5-T 2 . Inactivation of T 3 in the anterior pituitary might occur by deiodination at the tyrosyl ring via D1, thus terminating the stimulatory thyroid hormone signal in human somatomammotroph cells.

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Rapid stimulation of type I 5′-deiodinase in rat pituitaries by 3,3′,5-triiodo-l-thyronine

Cited by 47 publications

References 35 publications

Effects of proinflammatory cytokines on anterior pituitary 5'-deiodinase type I and type II

Effects of proinflammatory cytokines on anterior pituitary 5'-deiodinase type I and type II

Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

Type 1 deiodinase is stimulated by iodothyronines and involved in thyroid hormone metabolism in human somatomammotroph GX cells

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