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Journal ArticleDOI

Endogenous thyroid hormones modulate pituitary somatotroph differentiation during chicken embryonic development.

01 Jan 2004-Journal of Endocrinology (BioScientifica)-Vol. 180, Iss: 1, pp 45-53

TL;DR: Testing the hypothesis that endogenous thyroid hormones regulate the abundance of somatotrophs during chicken embryonic development indicated that treatment with exogenous thyroid hormones can modulate som atotroph abundance and that endogenous thyroxine and triiodothyronine treatment likely contributes to normal somatOTroph differentiation.

AbstractGrowth hormone cell differentiation normally occurs between day 14 and day 16 of chicken embryonic development. We reported previously that corticosterone (CORT) could induce somatotroph differentiation in vitro and in vivo and that thyroid hormones could act in combination with CORT to further augment the abundance of somatotrophs in vitro. The objective of the present study was to test our hypothesis that endogenous thyroid hormones regulate the abundance of somatotrophs during chicken embryonic development. Plasma samples were collected on embryonic day (e) 9–14. We found that plasma CORT and thyroid hormone levels increased progressively in mid-embryogenesis to e13 or e14, immediately before normal somatotroph differentiation. Administration of thyroxine (T4) and triiodothyronine (T3) into the albumen of fertile eggs on e11 increased somatotroph proportions prematurely on e13 in the developing chick embryos in vivo. Furthermore, administration of methimazole, the thyroid hormone synthesis inhibitor, on e9 inhibited somatotroph differentiation in vivo, as assessed on e14; this suppression was completely reversed by T 3 replacement on e11. Since we reported that T 3 alone was ineffective in vitro, we interpret these findings to indicate that the effects of treatments in vivo were due to interactions with endogenous glucocorticoids. These results indicate that treatment with exogenous thyroid hormones can modulate somatotroph abundance and that endogenous thyroid hormone synthesis likely contributes to normal somatotroph differentiation.

Topics: Hormone (58%), Thyroid (56%), Triiodothyronine (55%), Somatotropic cell (54%)

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Citations
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Journal ArticleDOI
F.M.Anne McNabb1
TL;DR: Thyroid function and its hypothalamic-pituitary-thyroid (HPT) axis control in birds is reviewed with emphasis on the similarities and differences in thyroid function compared to mammals and other vertebrate classes.
Abstract: This article reviews thyroid function and its hypothalamic-pituitary-thyroid (HPT) axis control in birds with emphasis on the similarities and differences in thyroid function compared to mammals and other vertebrate classes. Thyroid hormones are important in metabolism and the thermogenesis required for homeothermy in birds, as in mammals, the other homeothermic class of vertebrates. Thyroid hormones play important roles in development and growth in birds, as is the case for all vertebrate classes. The developmental effects of thyroid hormones in birds are presented in the context of differences in precocial and altricial patterns of development and growth with emphasis on oviparous development. The sections on thyroid hormone actions include discussion of effects on the development of a number of tissue types as well as on seasonal organismal processes and interactions of the thyroid axis with reproduction. The current picture of how environmental chemicals may disrupt avian thyroid function is relatively limited and is presented in the context of the assessment endpoints that have been used to date. These endpoints are categorized as thyroid and HPT axis endpoints versus target organ endpoints. The final section discusses two recommended assay protocols, the avian two-generation toxicity assay and the avian one-generation assay, and whether these protocols can evaluate thyroid disruption in birds.

172 citations


Cites background from "Endogenous thyroid hormones modulat..."

  • ...Recently thyroid hormones have been shown to affect the differentiation and abundance of somatotrophs in chicken embryos in vivo (Liu and Porter, 2004) and in vitro studies indicate this stimulation requires synergistic interactions with corticosterone (Liu et al., 2003)....

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Journal ArticleDOI
TL;DR: All embryonic tissues are exposed to relatively high doses of MMI and its oxidised metabolites, and the effect of maternal MMI treatment on embryonic thyroid hormone availability is most pronounced for brain T₃ content, which is reduced throughout the embryonic development period.
Abstract: Methimazole (MMI) is an anti-thyroid drug used in the treatment of chronic hyperthyroidism. There is, however, some debate about its use during pregnancy as MMI is known to cross the mammalian placenta and reach the developing foetus. A similar problem occurs in birds, where MMI is deposited in the egg and taken up by the developing embryo. To investigate whether maternally derived MMI can have detrimental effects on embryonic development, we treated laying hens with MMI (0.03% in drinking water) and measured total and reduced MMI contents in the tissues of hens and embryos at different stages of development. In hens, MMI was selectively increased in the thyroid gland, while its levels in the liver and especially brain remained relatively low. Long-term MMI treatment induced a pronounced goitre with a decrease in thyroxine (T₄) content but an increase in thyroidal 3,5,3'-triiodothyronine (T₃) content. This resulted in normal T₃ levels in tissues except in the brain. In chicken embryos, MMI levels were similar in the liver and brain. They gradually decreased during development but always remained above those in the corresponding maternal tissues. Contrary to the situation in hens, T₄ availability was only moderately affected in embryos. Peripheral T₃ levels were reduced in 14-day-old embryos but normal in 18-day-old embryos, while brain T₃ content was decreased at all embryonic stages tested. We conclude that all embryonic tissues are exposed to relatively high doses of MMI and its oxidised metabolites. The effect of maternal MMI treatment on embryonic thyroid hormone availability is most pronounced for brain T₃ content, which is reduced throughout the embryonic development period.

71 citations


Cites background from "Endogenous thyroid hormones modulat..."

  • ...It has been shown earlier that MMI is taken up from the egg by the embryo and is capable of disturbing development, including brain development (Iqbal et al. 1987, Liu & Porter 2004, Kagami & Nishigori 2010)....

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Journal ArticleDOI
TL;DR: This review focuses on the development of the thyrotropic, corticotropic and somatotropic axes in the chicken, emphasizing the central role of the pituitary gland in these endocrine systems.
Abstract: The ease of in vivo experimental manipulation is one of the main factors that have made the chicken embryo an important animal model in developmental research, including developmental endocrinology. This review focuses on the development of the thyrotropic, corticotropic and somatotropic axes in the chicken, emphasizing the central role of the pituitary gland in these endocrine systems. Functional maturation of the endocrine axes entails the cellular differentiation and acquisition of cell function and responsiveness of the different glands involved, as well as the establishment of top-down and bottom-up anatomical and functional communication between the control levels. Extensive cross-talk between the above-mentioned axes accounts for the marked endocrine changes observed during the last third of embryonic development. In a final paragraph we shortly discuss how genomic resources and new transgenesis techniques can increase the power of the chicken embryo model in developmental endocrinology research.

46 citations


Cites background from "Endogenous thyroid hormones modulat..."

  • ...Circulating CORT levels start to rise around day 14, most likely ecause of an increased secretion of ACTH at this time (Jenkins nd Porter, 2004)....

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  • ...mbryonic endocrine interior without triggering maternal intererence makes the chicken embryo a valuable model for the study f development and function of hormonal systems (Decuypere et l., 1990; Jenkins and Porter, 2004)....

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  • ...The appearance of hypothalamic CRH at this stage is accomanied by a marked increase in the number of corticotropes and i n r m ( Endocrinology 293 (2008) 17–24 19 ignificantly elevated plasma glucocorticoid levels (Wise and Frye, 973; Jenkins and Porter, 2004)....

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  • ...…as evidenced by the fact that in vivo CTH treatment increases the activity of the enzyme responsible for he conversion of pregnenolone to progesterone in adrenal glands rom 4-day-old embryos and stimulates corticosterone (CORT) prouction on day 5 of incubation (Jenkins and Porter, 2004)....

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  • ...By the end of the first week of incubation, both the thyroid nd the adrenal glands are supposedly functioning (see reviews by cNabb, 2007; Jenkins and Porter, 2004)....

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Journal ArticleDOI
TL;DR: A number of findings support the hypothesis that differentiation of these growth hormone (GH) producing cells in the chick and the rat is regulated by adrenal glucocorticoids and thyroid hormones, and a working model for the regulation of somatotroph differentiation during normal development includes modulation by elements of the hypothalamo-pituitary-adrenal and hypothalamo
Abstract: Anterior pituitary somatotroph differentiation occurs during chick embryonic and rat fetal development. A number of findings support the hypothesis that differentiation of these growth hormone (GH) producing cells in the chick and the rat is regulated by adrenal glucocorticoids and thyroid hormones. Somatotroph differentiation can be induced in cultures of chick embryonic and rat fetal pituitary cells with adrenal glucocorticoids and this effect can be modulated by concomitant treatment with thyroid hormones. Plasma levels of thyroid hormones, corticosterone and adrenocorticotropic hormone increase during development, consistent with the ontogeny of somatotrophs. Treatment of chick embryos or rat fetuses with glucocorticoids in vivo induces premature somatotroph differentiation, indicating that the adrenal gland, and ultimately anterior pituitary corticotrophs, may function to regulate pituitary GH cell differentiation during development. Administration of thyroid hormones in vivo also increases somatotrophs prematurely, and administration of the thyroid hormone synthesis inhibitor methimazole inhibits somatotroph differentiation in vivo, suggesting that endogenous thyroid hormone synthesis contributes to normal somatotroph differentiation. Our working model for the regulation of somatotroph differentiation during normal development includes modulation by elements of the hypothalamo–pituitary–adrenal and hypothalamo–pituitary–thyroid axes. Additional research is reviewed defining the mechanism of action for these peripheral hormones in induction of pituitary GH gene expression during development.

38 citations


Cites background from "Endogenous thyroid hormones modulat..."

  • ...During chick embryonic development, injection of T3 or T4 into the egg albumen on e9 increased GH cell numbers on e13 [40]....

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  • ...Thyroid hormone synthesis is required for normal somatotroph ontogeny, as inhibition of synthesis by the embryonic thyroid gland depresses somatotroph abundance during development [40]....

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  • ...Increased levels of CORT and ACTH have been documented to occur immediately before the increase in somatotroph abundance during normal development [3,25,40]....

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  • ...The ability of glucocorticoids to increase somatotrophs prematurely during development in vivo and to induce somatotroph differentiation in vitro is well documented in rats [21–23,26–28] and in chickens [24,30–33,35–37,40]....

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Journal ArticleDOI
TL;DR: There is evidence that, at least for some of these processes, THs may have similar roles in non-avian sauropsids, and how hatching-associated processes are regulated by hormones in these animals is not known.
Abstract: A major life stage transition in birds and other oviparous sauropsids is the hatching of the cleidoic egg. Not unlike amphibian metamorphosis, hatching in these species can be regarded as a transition from a relatively well-protected "aqueous" environment to a more hazardous and terrestrial life outside the egg, a transition in which thyroid hormones (THs) (often in concert with glucocorticoids) play an important role. In precocial birds such as the chicken, the perihatch period is characterized by peak values of THs. THs are implicated in the control of muscle development, lung maturation and the switch from chorioallantoic to pulmonary respiration, yolk sac retraction, gut development and induction of hepatic genes to accommodate the change in dietary energy source, initiation of thermoregulation, and the final stages of brain maturation as well as early post-hatch imprinting behavior. There is evidence that, at least for some of these processes, THs may have similar roles in non-avian sauropsids. In altricial birds such as passerines on the other hand, THs do not rise significantly until well after hatching and peak values coincide with the development of endothermy. It is not known how hatching-associated processes are regulated by hormones in these animals or how this developmental mode evolved from TH-dependent precocial hatching.

36 citations


Cites background from "Endogenous thyroid hormones modulat..."

  • ...Circulating corticosterone levels start to rise around E14 and act synergistically with THs on the differentiation of the growth hormone-producing cells in the pituitary gland (Jenkins and Porter, 2004; Liu and Porter, 2004; Porter, 2005)....

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References
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Journal ArticleDOI

267 citations


"Endogenous thyroid hormones modulat..." refers background in this paper

  • ...Multiple studies suggest that thyroid hormones can activate GH synthesis in adult rats and synergistically stimulate somatotroph abundance with glucocorticoids in rat pituitary cell lines (Hervas et al. 1975, Shapiro et al. 1978, Dobner et al. 1981, Spindler et al. 1982, Yaffe & Samuels 1984)....

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Journal ArticleDOI
TL;DR: The studies suggest that regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes.
Abstract: Using cultured GH1 cells, we reported that stimulation (3- to 5-fold) of growth hormone synthesis and mRNA levels by thyroid hormone is mediated by a chromatin-associated receptor. Thyroid hormone also elicits a rapid reduction of homologous receptor in GH1 cells primarily by decreasing the synthetic rate of receptor ( Raaka , B. M., and Samuels , H. H. (1981) J. Biol. Chem. 256, 6883-6889). Without 3,5,3'-triiodo-L-thyronine (L-T3), glucocorticoid agonists induced a limited and delayed effect while L-T3 + glucocorticoid synergistically stimulated the response an additional 2- to 4-fold compared to L-T3. In this study, we utilized GC cells, a related cell line, to compare the abundance of L-T3-receptor complexes to the rate of growth hormone mRNA synthesis and gene transcription. Gene transcription was assessed by in vitro labeling of nuclei with [alpha-32P]UTP which were derived from cells incubated with hormone(s), while mRNA synthesis was determined in intact cells by [3H]uridine labeling. Labeled growth hormone mRNA and gene transcripts were quantitated by filter hybridization to plasmid containing growth hormone cDNA. L-T3 rapidly decreased receptor levels in GC cells with kinetics similar to that in GH1 cells. Both the L-T3 and the synergistic L-T3 + glucocorticoid stimulation of growth hormone mRNA synthesis changed in parallel with the level of L-T3-receptor complexes. Glucocorticoid hormones alone elicited a variable response which resulted in minimal stimulation or inhibition of growth hormone mRNA synthesis or gene transcription rates. No apparent lag was identified between the kinetics of L-T3 binding to receptor and stimulation of growth hormone gene transcription. L-T3 stimulated growth hormone gene transcription rates maximally in 1 h which then progressively decreased in parallel with L-T3-receptor levels. Using [3H]uridine pulse-chase, growth hormone mRNA was found to have a half-life of approximately 50 h in agreement with the decay curve of growth hormone production of deinduced cells. Our studies suggest that regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes.

257 citations


"Endogenous thyroid hormones modulat..." refers background in this paper

  • ...Multiple studies suggest that thyroid hormones can activate GH synthesis in adult rats and synergistically stimulate somatotroph abundance with glucocorticoids in rat pituitary cell lines (Hervas et al. 1975, Shapiro et al. 1978, Dobner et al. 1981, Spindler et al. 1982, Yaffe & Samuels 1984)....

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Journal ArticleDOI
TL;DR: It is shown that incubation of GH3 cells with a thyroid hormone, a glucocorticoid hormone, or both hormones caused an increase of cytoplasmic pre-GH mRNA sequences of about 4, 22, and 13-fold, respectively, and 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 cy toplasm.
Abstract: 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 of the 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-GH1) 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.

202 citations


"Endogenous thyroid hormones modulat..." refers background in this paper

  • ...Multiple studies suggest that thyroid hormones can activate GH synthesis in adult rats and synergistically stimulate somatotroph abundance with glucocorticoids in rat pituitary cell lines (Hervas et al. 1975, Shapiro et al. 1978, Dobner et al. 1981, Spindler et al. 1982, Yaffe & Samuels 1984)....

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Journal ArticleDOI
TL;DR: The mea-urement by RIA of changes in GH content of the rat pituitary may provide the most adequate parameter available at present for a biological effect in vivo of single doses of the thyroid hormones, a measurement clearly related to an important physiological role.
Abstract: The effects of thyroid hormone deprivation and restitution on growth hormone (GH) economy have been studied in the rat by means of a specific radioimmunoassay. The pituitary GH content and the plasma GH levels before and during stimulation with pentobarbital (“PB-test”) were studied in male rats at different intervals after surgical thyroidectomy (Ť), and in Ť rats at different time intervals after the ip injection of 0.20,1.75, and 5.0 µgthyroxine (T4) or 0.05, 0.10, 0.20 and 1.0 µg triiodothyronine (T3),all doses being referred to 100 g body wt. Pituitary GH content decreased very rapidly after Ť, a difference being shown at the end of the shortest time interval studied (24 h); 24 days after Ť, pituitary GH content was 0.3% or less of the pre-Ť level, the basal plasma GH was lower than in intact controls and an increase in plasma GH during PB-stimulation wasno longer observed. When rats Ť for 30 days or longer were injected once with T4or T3, pituitary GH content increased; basal plasma GH levels increa...

190 citations


"Endogenous thyroid hormones modulat..." refers background in this paper

  • ...Multiple studies suggest that thyroid hormones can activate GH synthesis in adult rats and synergistically stimulate somatotroph abundance with glucocorticoids in rat pituitary cell lines (Hervas et al. 1975, Shapiro et al. 1978, Dobner et al. 1981, Spindler et al. 1982, Yaffe & Samuels 1984)....

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Journal ArticleDOI
TL;DR: Quantitation of growth hormone mRNA levels by cell-free protein synthesis demonstrates that the regulation ofgrowth hormone synthesis by thyroid and glucocorticoid hormones is explained by a synergistic pretranslational control mechanism, presumably at the level of the growth hormone gene.
Abstract: We have previously demonstrated that thyroid hormone controls growth hormone synthesis in GH1 cells and that the induction of the growth hormone response by glucocorticoid appears to be highly dependent on thyroid hormone action. Thyroid hormone induces growth hormone synthesis approximately 5- to 20-fold and cortisol increases this response 2- to 6-fold further. Long-term kinetics of the growth hormone response show that, without added thyroid hormone, cortisol can induce a small-growth hormone response after 48 hr of incubation. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis of proteins synthesized in intact cells demonstrates that the cortisol enhancement of growth hormone synthesis in cells incubated with thyroid hormone is a relatively selective process. Quantitation of growth hormone mRNA levels by cell-free protein synthesis demonstrates that the regulation of growth hormone synthesis by thyroid and glucocorticoid hormones is explained by a synergistic pretranslational control mechanism, presumably at the level of the growth hormone gene.

165 citations


"Endogenous thyroid hormones modulat..." refers background in this paper

  • ...Multiple studies suggest that thyroid hormones can activate GH synthesis in adult rats and synergistically stimulate somatotroph abundance with glucocorticoids in rat pituitary cell lines (Hervas et al. 1975, Shapiro et al. 1978, Dobner et al. 1981, Spindler et al. 1982, Yaffe & Samuels 1984)....

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