scholarly journals Selective labelling and inactivation of creatine kinase isoenzymes by the thyroid hormone derivative N-bromoacetyl-3,3′,5-tri-iodo-l-thyronine

1993 ◽  
Vol 291 (2) ◽  
pp. 463-472 ◽  
Author(s):  
M Wyss ◽  
T Wallimann ◽  
J Köhrle
Keyword(s):  
Creatine Kinase ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Rat Heart ◽  
Covalent Modification ◽  
Regulation Of Transcription ◽  
Selective Labelling ◽  
Mitochondrial Fractions

Besides their well-known regulation of transcription by binding to nuclear receptors, thyroid hormones have been suggested to have direct effects on mitochondria. In a previous study, incubation of rat heart mitochondria with 125I-labelled N-bromoacetyl-3,3′,5-tri-iodo-L-thyronine (BrAcT3), a thyroid hormone derivative with an alkylating side chain, resulted in the selective labelling of a protein doublet around M(r) 45,000 on SDS/polyacrylamide gels [Rasmussen, Köhrle, Rokos and Hesch (1989) FEBS Lett. 255, 385-390]. Now, this protein doublet has been identified as mitochondrial creatine kinase (Mi-CK). Immunoblotting experiments with the cytoplasmic and mitochondrial fractions of rat heart, brain and liver, as well as inactivation studies with the purified chicken CK isoenzymes have further demonstrated that all four CK isoenzymes (Mia-, Mib-, M- and B-CK) are indeed selectively labelled by BrAcT3. However, in contrast with their bromoalkyl derivatives, thyroid hormones themselves did not compete for CK labelling, suggesting that not the thyroid hormone moiety but rather the bromoacetyl-driven alkylation of the highly reactive ‘essential’ thiol group of CK accounts for this selective labelling. Therefore the assumption that CK isoenzymes are thyroid-hormone-binding proteins has to be dismissed. Instead, bromoacetyl-based reagents may allow a very specific covalent modification and inactivation of CK isoenzymes in vitro and in vivo.

scholarly journals Thyroid hormone increases beta‐catenin levels through PI3K in rat heart in vivo and in vitro

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Marcela Sorelli Carneiro‐Ramos ◽  
Gabriela Placoná Diniz ◽  
Maria Luiza Morais Barreto‐Chaves ◽  
Anselmo Sigari Moriscot
Keyword(s):  
Thyroid Hormone ◽  
Rat Heart ◽  
Beta Catenin

scholarly journals Endogenous thyroid hormones modulate pituitary somatotroph differentiation during chicken embryonic development

2004 ◽  
Vol 180 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L Liu ◽  
TE Porter
Keyword(s):  
Thyroid Hormone ◽  
Embryonic Development ◽  
Thyroid Hormones ◽  
Synthesis Inhibitor ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis ◽  
Growth Hormone Cell ◽  
Thyroid Hormone Levels

Growth 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 e 13 or e 14, immediately before normal somatotroph differentiation. Administration of thyroxine (T4) and triiodothyronine (T3) into the albumen of fertile eggs on e 11 increased somatotroph proportions prematurely on e 13 in the developing chick embryos in vivo. Furthermore, administration of methimazole, the thyroid hormone synthesis inhibitor, on e 9 inhibited somatotroph differentiation in vivo, as assessed on e 14; this suppression was completely reversed by T3 replacement on e 11. Since we reported that T3 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.

scholarly journals Thyroid Hormone Receptor α1 Directly Controls Transcription of the β-Catenin Gene in Intestinal Epithelial Cells

2006 ◽  
Vol 26 (8) ◽  
pp. 3204-3214 ◽  
Author(s):  
Michelina Plateroti ◽  
Elsa Kress ◽  
Jun Ichirou Mori ◽  
Jacques Samarut
Keyword(s):  
Thyroid Hormone ◽  
Epithelial Cell ◽  
Thyroid Hormones ◽  
Transcriptional Control ◽  
Thyroid Hormone Receptor ◽  
Intestinal Epithelial ◽  
Type D ◽  
Hormone Responsive Element

ABSTRACT Thyroid hormones, T3 and T4, are known regulators of intestine development. The best characterized example is the remodeling of the gastrointestinal tract during amphibian metamorphosis. Thyroid hormones act via nuclear receptors, the TRs, which are T3-dependent transcription factors. We previously showed that intestinal epithelial cell proliferation is controlled by thyroid hormones and the TRα gene. To analyze the mechanisms responsible, we studied the expression of genes belonging to and/or activated by the Wnt/β-catenin pathway, a major actor in the control of physiological and pathological epithelial proliferation in the intestine. We show that T3-TRα1 controls the transcription of the β-catenin gene in an epithelial cell-autonomous way. This is parallel to positive regulation of proliferation-controlling genes such as type D cyclins and c-myc, known targets of the Wnt/β-catenin. In addition, we show that the regulation of the β-catenin gene is direct, as TR binds in vitro and in chromatin in vivo to a specific thyroid hormone-responsive element present in intron 1 of this gene. This is the first report concerning in vivo transcriptional control of the β-catenin gene. As Wnt/β-catenin plays a crucial role in intestinal tumorigenesis, our observations open a new perspective on the study of TRs as potential tumor inducers.

The effect of triiodothyronine on cyclic AMP, phosphorylase, and adenyl cyclase in rat heart

1969 ◽  
Vol 47 (11) ◽  
pp. 913-916 ◽  
Author(s):  
John H. McNeill ◽  
Lawrence D. Muschek ◽  
Theodore M. Brody
Keyword(s):  
Thyroid Hormone ◽  
Cyclic Amp ◽  
Rat Heart ◽  
Adenyl Cyclase

Pretreatment with triiodothyronine (T3) greatly enhanced the epinephrine-induced increase in rat cardiac phosphorylase a. T3 treatment, however, did not increase the level of adenosine-3′,5′-monophosphate (cyclic AMP) in rat heart. T3 treatment also did not increase the activity of rat heart adenyl cyclase or change the sensitivity of the enzyme to epinephrine when activity was determined in vitro. It is suggested that if thyroid hormone affects the activity of adenyl cyclase in vivo the effect is lost in the preparation of the enzyme for assay in vitro.

Effects of thyroid hormones on cartilage sulphation in sex-linked dwarf chickens

1989 ◽  
Vol 121 (1) ◽  
pp. 107-111 ◽  
Author(s):  
S. Hoshino ◽  
M. Wakita ◽  
Y. Kobayashi ◽  
T. Kakegawa ◽  
M. Suzuki
Keyword(s):  
Growth Rate ◽  
Growth Factor ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Chick Embryos ◽  
Chicken Serum ◽  
Factor I ◽  
Dwarf Chicken

Abstract. The present investigation was undertaken to see if exogenous thyroid hormone could stimulate cartilage sulphation in vivo and in vitro in sex-linked dwarf chickens. L-thyroxine or L-3,5,3'-triiodothyronine injection for 7 consecutive days stimulated in vivo 35SO2−4 incorporation into trachea cartilages of the dwarf chicken. Both thyroid hormones added to the incubation medium with or without 2.5% dwarf chicken serum also stimulated in vitro 35SO2−4 incorporation into pelvic rudiment from 11-day chick embryos. These data demonstrate that thyroid hormones, like insulin-like growth factor I, might be responsible for the reduced growth rate of dwarf chickens.

scholarly journals Direct Regulation of Mitochondrial RNA Synthesis by Thyroid Hormone

1999 ◽  
Vol 19 (1) ◽  
pp. 657-670 ◽  
Author(s):  
José A. Enríquez ◽  
Patricio Fernández-Silva ◽  
Nuria Garrido-Pérez ◽  
Manuel J. López-Pérez ◽  
Acisclo Pérez-Martos ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Transcription Initiation ◽  
Dimethyl Sulfate ◽  
Nuclear Genes ◽  
Regulation Of Transcription ◽  
Mitochondrial Rna ◽  
Mitochondrial Transcription ◽  
In Organello

ABSTRACT We have analyzed the influence of in vivo treatment and in vitro addition of thyroid hormone on in organello mitochondrial DNA (mtDNA) transcription and, in parallel, on the in organello footprinting patterns at the mtDNA regions involved in the regulation of transcription. We found that thyroid hormone modulates mitochondrial RNA levels and the mRNA/rRNA ratio by influencing the transcriptional rate. In addition, we found conspicuous differences between the mtDNA dimethyl sulfate footprinting patterns of mitochondria derived from euthyroid and hypothyroid rats at the transcription initiation sites but not at the mitochondrial transcription termination factor (mTERF) binding region. Furthermore, direct addition of thyroid hormone to the incubation medium of mitochondria isolated from hypothyroid rats restored the mRNA/rRNA ratio found in euthyroid rats as well as the mtDNA footprinting patterns at the transcription initiation area. Therefore, we conclude that the regulatory effect of thyroid hormone on mitochondrial transcription is partially exerted by a direct influence of the hormone on the mitochondrial transcription machinery. Particularly, the influence on the mRNA/rRNA ratio is achieved by selective modulation of the alternative H-strand transcription initiation sites and does not require the previous activation of nuclear genes. These results provide the first functional demonstration that regulatory signals, such as thyroid hormone, that modify the expression of nuclear genes can also act as primary signals for the transcriptional apparatus of mitochondria.

Insight into the physiological actions of thyroid hormone receptors from genetically modified mice

2002 ◽  
Vol 175 (3) ◽  
pp. 553-570 ◽  
Author(s):  
PJ O'Shea ◽  
GR Williams
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Genetically Modified ◽  
Receptor Protein ◽  
Mrna Isoforms ◽  
Iodothyronine Deiodinase ◽  
Thyrotrophin Releasing Hormone ◽  
Genetically Modified Mice

Thyroid hormones exert a range of developmental and physiological actions in all vertebrates. Serum concentrations of L-thyroxine (T4) and 3,5,3 -L-triiodothyronine (T3) are maintained by a negative feedback loop involving T3-inhibition of hypothalamic thyrotrophin releasing hormone (TRH) and pituitary thyroid stimulating hormone (TSH) secretion, and by tissue specific and hormone-regulated expression of the three iodothyronine deiodinase enzymes that activate or metabolise thyroid hormones. T3 actions are mediated by two T3-receptors, TRalpha and TRbeta, which act as hormone-inducible transcription factors. The TRalpha (NR1A1) and TRbeta (NR1A2) genes encode mRNAs that are alternatively spliced to generate 9 mRNA isoforms (TRalpha1, alpha2, alpha3, Deltaalpha1, Deltaalpha2, beta1, beta2, beta3 and Deltabeta3), of which four (TRalpha1, alpha2, beta1 and beta2) are known to be expressed at the protein level in vivo. The numerous TR mRNAs are expressed widely in tissue- and developmental stage-specific patterns, although it is important to note that levels of mRNA expression may not correlate with receptor protein concentrations in individual tissues. The TRalpha2, alpha3, Deltaalpha1 and Deltaalpha2 transcripts encode proteins that fail to bind T3 in vitro. These non-binding isoforms, in addition to TRDeltabeta3 which does bind hormone, may act as dominant negative antagonists of the true T3-binding receptors in vitro, but their physiological functions and those of the TRbeta3 isoform have not been determined. In order to obtain a new understanding of the complexities of T3 action in vivo and the role of TRs during development, many mouse models of disrupted or augmented thyroid hormone signalling have been generated. The aim of this review is to provide a picture of the physiological actions of thyroid hormones by considering the phenotypes of these genetically modified mice.

scholarly journals Influence of thyroid hormone on the in vitro translational activity of specific mRNAs in the rat heart.

1983 ◽  
Vol 258 (12) ◽  
pp. 7738-7745 ◽  
Author(s):  
W H Dillmann ◽  
A Barrieux ◽  
W E Neeley ◽  
P Contreras
Keyword(s):  
Thyroid Hormone ◽  
Rat Heart ◽  
Translational Activity ◽  
Specific Mrnas
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