scholarly journals Altricial bird early-stage embryos express the molecular "machinery" to respond to maternal thyroid hormone cues

2021 ◽  
Author(s):  
Suvi Ruuskanen ◽  
Mikaela Hukkanen ◽  
Natacha Garcin ◽  
Nina Cossin-Sevrin ◽  
Bin-Yan Hsu ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Ecological Model ◽  
Thyroid Hormone Receptor ◽  
Early Stage ◽  
Biologically Active ◽  
Cyanistes Caeruleus ◽  
Molecular Machinery ◽  
Altricial Birds ◽  
Maternal Thyroid

Maternal hormones, such as thyroid hormones transferred to embryos and eggs, are key signalling pathways to mediate maternal effects. To be able to respond to maternal cues, embryos must express key molecular "machinery" of the hormone pathways, such as enzymes and receptors. While altricial birds begin thyroid hormone (TH) production only at/after hatching, experimental evidence suggests that their phenotype can be influenced by maternal THs deposited in the egg. However, it is not understood, how and when altricial birds express genes in the TH-pathway. For the first time, we measured the expression of key TH-pathway genes in altricial embryos, using two common altricial ecological model species (pied flycatcher, Ficedula hypoleuca and blue tit Cyanistes caeruleus). Deiodinase DIO1 gene expression could not be reliably confirmed in either species, but deiodinase enzyme DIO2 and DIO3 genes were expressed in both species. Given that DIO2 coverts T4 to biologically active T3, and DIO3 mostly T3 to inactive forms of thyroid hormones, our results suggest that embryos may modulate maternal signals. Thyroid hormone receptor (THRA and THRB) and monocarboxyl membrane transporter gene (SLC15A2) were also expressed, enabling TH-responses. Our results suggest that early altricial embryos may be able to respond and potentially modulate maternal signals conveyed by thyroid hormones.

Regulation of Mammary Gland Sensitivity to Thyroid Hormones During the Transition from Pregnancy to Lactation

2008 ◽  
Vol 233 (10) ◽  
pp. 1309-1314 ◽  
Author(s):  
A. V. Capuco ◽  
E. E. Connor ◽  
D. L. Wood
Keyword(s):  
Mammary Gland ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Hormone Receptor ◽  
Physiological State ◽  
Expression Patterns ◽  
Type I ◽  
Hormone Activity ◽  
Iodothyronine Deiodinase ◽  
Copy Numbers

Thyroid hormones are galactopoietic and help to establish the mammary gland’s metabolic priority during lactation. Expression patterns for genes that can alter tissue sensitivity to thyroid hormones and thyroid hormone activity were evaluated in the mammary gland and liver of cows at 53, 35, 20, and 7 days before expected parturition, and 14 and 90 days into the subsequent lactation. Transcript abundance for the three isoforms of iodothyronine deiodinase, type I ( DIO1), type II ( DIO2) and type III ( DIO3), thyroid hormone receptors alpha1 ( TRα 1), alpha2 ( TRα 2) and beta1 ( TRβ 1), and retinoic acid receptors alpha ( RXRα) and gamma ( RXRγ), which act as coregulators of thyroid hormone receptor action, were evaluated by quantitative RT-PCR. The DIO3 is a 5-deiodinase that produces inactive iodothyronine metabolites, whereas DIO1 and DIO2 generate the active thyroid hormone, triiodothyronine, from the relatively inactive precursor, thyroxine. Low copy numbers of DIO3 transcripts were present in mammary gland and liver. DIO2 was the predominant isoform expressed in mammary gland and DIO1 was the predominant isoform expressed in liver. Quantity of DIO1 mRNA in liver tissues did not differ with physiological state, but tended to be lowest during lactation. Quantity of DIO2 mRNA in mammary gland increased during lactation ( P < 0.05), with copy numbers at 90 days of lactation 6-fold greater than at 35 and 20 days prepartum. When ratios of DIO2/DIO3 mRNA were evaluated, the increase was more pronounced (>100-fold). Quantity of TRβ 1 mRNA in mammary gland increased with onset of lactation, whereas TRα 1 and TRα 2 transcripts did not vary with physiological state. Conversely, quantity of RXRα mRNA decreased during late gestation to low levels during early lactation. Data suggest that increased expression of mammary TRβ 1 and DIO2, and decreased RXRα, provide a mechanism to increase thyroid hormone activity within the mammary gland during lactation.

scholarly journals Hypercholesterolemia in Two Siblings with Resistance to Thyroid Hormones Due to Disease-Causing Variant in Thyroid Hormone Receptor (THRB) Gene

Medicina ◽  
2020 ◽  
Vol 56 (12) ◽  
pp. 699
Author(s):  
Maja Pajek ◽  
Magdalena Avbelj Stefanija ◽  
Katarina Trebusak Podkrajsek ◽  
Jasna Suput Omladic ◽  
Mojca Zerjav Tansek ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Pathogenic Mutation ◽  
Laboratory Findings ◽  
Cholesterol Levels ◽  
Resistance To Thyroid Hormones ◽  
Hormonal Resistance ◽  
Disease Variant

Resistance to thyroid hormone beta (RTHβ) is a syndrome characterized by a reduced response of target tissues to thyroid hormones. In 85% of cases, a pathogenic mutation in the thyroid hormone receptor beta (THRB) gene is found. The clinical picture of RTHβ is very diverse; the most common findings are goiter and tachycardia, but the patients might be clinically euthyroid. The laboratory findings are almost pathognomonic with elevated free thyroxin (fT4) levels and high or normal thyrotropin (TSH) levels; free triiodothyronin (fT3) levels may also be elevated. We present three siblings with THRB mutation (heterozygous disease-variant c.727C>T, p.Arg243Trp); two of them also had hypercholesterolemia, while all three had several other clinical characteristics of RTHβ. This is the first description of the known Slovenian cases with RTHβ due to the pathogenic mutation in the THRB gene. Hypercholesterolemia might be etiologically related with RTHβ, since the severity of hormonal resistance varies among different tissues and hypercholesterolemia in patients with THRB variants might indicate the relatively hypothyroid state of the liver. We suggest that cholesterol levels are measured in all RTHβ patients.

scholarly journals Athyroid Pax8−/− Mice Cannot Be Rescued by the Inactivation of Thyroid Hormone Receptor α1

Endocrinology ◽  
2005 ◽  
Vol 146 (7) ◽  
pp. 3179-3184 ◽  
Author(s):  
Jens Mittag ◽  
Sönke Friedrichsen ◽  
Heike Heuer ◽  
Silke Polsfuss ◽  
Theo J. Visser ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Postnatal Life ◽  
Mrna Levels ◽  
Negative Effects ◽  
Double Knockout ◽  
Short Life Span ◽  
Knockout Animals

Abstract The Pax8−/− mouse provides an ideal animal model to study the consequences of congenital hypothyroidism, because its only known defect is the absence of thyroid follicular cells. Pax8−/− mice are, therefore, completely athyroid in postnatal life and die around weaning unless they are substituted with thyroid hormones. As reported recently, Pax8−/− mice can also be rescued and survive to adulthood by the additional elimination of the entire thyroid hormone receptor α (TRα) gene, yielding Pax8−/−TRαo/o double-knockout animals. This observation has led to the hypothesis that unliganded TRα1 might be responsible for the lethal phenotype observed in Pax8−/− animals. In this study we report the generation of Pax8−/−TRα1−/− double-knockout mice that still express the non-T3-binding TR isoforms α2 and Δα2. These animals closely resemble the phenotype of Pax8−/− mice, including growth retardation and a completely distorted appearance of the pituitary with thyrotroph hyperplasia and hypertrophy, extremely high TSH mRNA levels, reduced GH mRNA expression, and the almost complete absence of lactotrophs. Like Pax8−/− mice, Pax8−/−TRα1−/− compound mutants die around weaning unless they are substituted with thyroid hormones. These findings do not support the previous interpretation that the short life span of Pax8−/− mice is due to the negative effects of the TRα1 aporeceptor, but, rather, suggest a more complex mechanism involving TRα2 and an unliganded TR isoform.

scholarly journals Molecular cloning and characterization of thyroid hormone receptors in teleost fish

2001 ◽  
Vol 26 (1) ◽  
pp. 51-65 ◽  
Author(s):  
O Marchand ◽  
R Safi ◽  
H Escriva ◽  
E Van Rompaey ◽  
P Prunet ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Teleost Fish ◽  
Hormone Receptor ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Hormone Response Elements ◽  
Reverse Transcription Pcr ◽  
Wide Range

Thyroid hormones are pleiotropic factors important for many developmental and physiological functions in vertebrates. Their effects are mediated by two specific receptors (TRalpha and TRbeta) which are members of the nuclear hormone receptor superfamily. To clarify the function of these receptors, our laboratory has started a comparative study of their role in teleost fish. This type of approach has been hampered by the isolation of specific clones for each fish species studied. In this report, we describe an efficient reverse transcription/PCR procedure that allows the isolation of large fragments corresponding to TRalpha and TRbeta of a wide range of teleost fish. Phylogenetic analysis of these receptors revealed a placement consistent with their origin, sequences from teleost fish being clearly monophyletic for both TRalpha and TRbeta. Interestingly, this approach allowed us to isolate (from tilapia and salmon) several new TRalpha or TRbeta isoforms resulting from alternative splicing. These isoforms correspond to expressed transcripts and thus may have an important physiological function. In addition, we isolated a cDNA encoding TRbeta in the Atlantic salmon (Salmo salar) encoding a functional thyroid hormone receptor which binds specific thyroid hormone response elements and regulates transcription in response to thyroid hormones.

scholarly journals Isolation of a cDNA clone encoding a biologically active thyroid hormone receptor.

1988 ◽  
Vol 85 (14) ◽  
pp. 5031-5035 ◽  
Author(s):  
R. J. Koenig ◽  
R. L. Warne ◽  
G. A. Brent ◽  
J. W. Harney ◽  
P. R. Larsen ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Cdna Clone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Biologically Active

scholarly journals Hematopoiesis in aged female mice devoid of thyroid hormone receptors

2020 ◽  
Vol 244 (1) ◽  
pp. 83-94 ◽  
Author(s):  
Ángela Sánchez ◽  
Constanza Contreras-Jurado ◽  
Diego Rodríguez ◽  
Javier Regadera ◽  
Susana Alemany ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
B Cell ◽  
Knockout Mice ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Dominant Negative ◽  
Thyroid Hormone Receptors ◽  
Female Mice

Hypothyroidism is often associated with anemia and immunological disorders. Similar defects are found in patients and in mice with a mutated dominant-negative thyroid hormone receptor α (TRα) and in knockout mice devoid of this receptor, suggesting that this isoform is responsible for the effects of the thyroid hormones in hematopoiesis. However, the hematological phenotype of mice lacking also TRβ has not yet been examined. We show here that TRα1/TRβ-knockout female mice, lacking all known thyroid hormone receptors with capacity to bind thyroid hormones, do not have overt anemia and in contrast with hypothyroid mice do not present reduced Gata1 or Hif1 gene expression. Similar to that found in hypothyroidism or TRα deficiency during the juvenile period, the B-cell population is reduced in the spleen and bone marrow of ageing TRα1/TRβ-knockout mice, suggesting that TRβ does not play a major role in B-cell development. However, splenic hypotrophy is more marked in hypothyroid mice than in TRα1/TRβ-knockout mice and the splenic population of T-lymphocytes is not significantly impaired in these mice in contrast with the reduction found in hypothyroidism. Our results show that the overall hematopoietic phenotype of the TRα1/TRβ-knockout mice is milder than that found in the absence of hormone. Although other mechanism/s cannot be ruled out, our results suggest that the unoccupied TRs could have a negative effect on hematopoiesis, likely secondary to repression of hematopoietic gene expression.

Causes and laboratory investigation of hypothyroidism

2011 ◽  
pp. 530-537 ◽  
Author(s):  
Ferruccio Santini ◽  
Aldo Pinchera
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Thyroid Hormone Receptor ◽  
Hormone Secretion ◽  
Thyroid Tissue ◽  
Clinical Manifestations ◽  
Primary Hypothyroidism ◽  
Central Hypothyroidism ◽  
Resistance To Thyroid Hormones

Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).

scholarly journals Thyroid hormone resistance syndrom: difficulties in differential diagnosis

2018 ◽  
Vol 14 (1) ◽  
pp. 39-46
Author(s):  
Lyudmila A. Ruyatkina ◽  
Aguniya A. Molchanova ◽  
Alina S. Ruyatkina ◽  
Lyudmila Y. Rozhinskaya
Keyword(s):  
Differential Diagnosis ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Hormone Receptor ◽  
Signs And Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Heterozygous Mutation ◽  
Hormone Resistance ◽  
Thyroid Hormone Resistance ◽  
Free Thyroid Hormones

Thyroid hormone resistance syndrome (RTH) is a rare disorder characterized by reduced peripheral tissue responses to thyroid hormones (TH) and elevated levels of circulating free thyroid hormones. Resistance to thyroid hormone is caused by mutations of the thyroid hormone receptor beta (THRB) gene. In this article, we present case of 26-years-old women who presented with unclear signs and symptoms. Thyroid morphology and function were evaluated with standard ultrasound of the thyroid, scintigraphy and cytological specimen obtained by FNAB. The features of the basic assessment of thyroid status with an emphasis on the concept of “±feedback” of thyroid-stimulating hormone (TSH) and TH. A differential diagnosis of TSH-secreting pituitary adenoma and RTH was discussed. Heterozygous mutation p.P453T in the THRB gene was detected. Thus, the given clinical case demonstrates the necessity of the thorough examination of patients in identifying disorders of the principle of “±feedback”. The observation in dynamics is recommended.

scholarly journals The Diurnal Variation of Thyroid Hormones in Individuals Attending Tertiary Care Hospital, Kanchipuram District

2020 ◽  
Vol 13 (4) ◽  
pp. 1729-1735
Author(s):  
Santhosh Viswan ◽  
Gurulakshmi Gurusamy ◽  
Khadeja Bi Altaff ◽  
Suganya Subbarayalu ◽  
Gomathi Surendran
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Tertiary Care ◽  
Biologically Active ◽  
Enzyme Linked Immunosorbent Assay ◽  
P Value ◽  
Care Hospital ◽  
Cross Sectional ◽  
Free Thyroid Hormones ◽  
The Mean

Free thyroxin hormones FT4 and FT3 are unbounded thyroid hormone are biologically active and involves in regulation of metabolism. Measuring the concentrations of free thyroid hormones is of great diagnostic value. A cross sectional study was carried out during the March 2019 to September 2019 in patients between 18 years to 60 years. A total of 60 samples were collected from 30 patients attending Karpaga Vinayaga Institute of Medical Sciences at morning (6am-8am) and 2nd sampling at night (8pm-9pm). FT4, FT3 and TSH were measured by Enzyme linked immunosorbent assay, using Avantor kit.In our study 36.67% participants were males, 63.3% participants were females. The mean FT3, FT4 and TSH in day are 2.43±0.56, 1.14±0.44 and 2.74±3.16 respectively. The mean night FT3, FT4 and TSH are 2.66±0.55, 1.3±0.61 and 3.21±3.18 respectively. The one sample t test shows difference of FT3, t 4.489 and p value 0.000, FT4, t value 3.092 and p value 0.004 and TSH t value 3.394 and p value 0.002. The time of blood sampling has an important role in the interpretation of TSH levels. However fluctuations in diurnal variations in thyroid hormone levels are less. In our study although statistically significant, all the values are within the normal biological reference interval Further studies in larger cohorts is essential to desire important conclusions.

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