scholarly journals Prolonged food deprivation increases mRNA expression of deiodinase 1 and 2, and thyroid hormone receptor  -1 in a fasting-adapted mammal

2013 ◽  
Vol 216 (24) ◽  
pp. 4647-4654 ◽  
Author(s):  
B. Martinez ◽  
J. G. Sonanez-Organis ◽  
J. P. Vazquez-Medina ◽  
J. A. Viscarra ◽  
D. S. MacKenzie ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Food Deprivation ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor

scholarly journals Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

2007 ◽  
Vol 195 (3) ◽  
pp. 429-438 ◽  
Author(s):  
C R Liu ◽  
L Y Li ◽  
F Shi ◽  
X Y Zang ◽  
Y M Liu ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Developmental Process ◽  
Control Group ◽  
Rat Myocardium ◽  
Receptor Mrna ◽  
Close Relationship ◽  
Heart Lesions

Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNA was extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRα1 mRNA expression was upregulated by 51% (P<0.01), TRα2 mRNA expression was downregulated by 58% (P<0.01), and TRβ1 mRNA expression remained unchanged in hyperthyroid rat myocardium (P>0.05). TRα1, TRα2, and TRβ1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRα1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRα2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRβ1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.

scholarly journals Differential effects of leptin and refeeding on the fasting-induced decrease of pituitary type 2 deiodinase and thyroid hormone receptor β2 mRNA expression in mice

2006 ◽  
Vol 190 (2) ◽  
pp. 537-544 ◽  
Author(s):  
A Boelen ◽  
J Kwakkel ◽  
X G Vos ◽  
W M Wiersinga ◽  
E Fliers
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Hormone Metabolism ◽  
Serum Leptin ◽  
Thyroid Hormone Metabolism ◽  
Hpt Axis ◽  
As Effects

Profound changes in thyroid hormone metabolism occur in the central part of the hypothalamus–pituitary–thyroid (HPT) axis during fasting. Hypothalamic changes are partly reversed by leptin administration, which decreases during fasting. It is unknown to what extent leptin affects the HPT axis at the level of the pituitary. We, therefore, studied fasting-induced alterations in pituitary thyroid hormone metabolism, as well as effects of leptin administration on these changes. Because refeeding rapidly increased serum leptin, the same parameters were studied after fasting followed by refeeding. Fasting for 24 h decreased serum T3 and T4 and pituitary TSHβ, type 2deiodinase (D2), and thyroid hormone receptor β2 (TRβ2) mRNA expression. The decrease in D2 and TRβ2 mRNA expression was prevented when 20 μg leptin was administered twice during fasting. By contrast, the decrease in TSHβ mRNA expression was unaffected. A single dose of leptin given after 24 h fasting did not affect decreased TSHβ, D2, and TRβ2 mRNA expression, while 4 h refeeding resulted in pituitary D2 and TRβ2 mRNA expression as observed in control mice. Serum leptin, T3, and T4 after refeeding were similar compared with leptin administration. We conclude that fasting decreases pituitary TSHβ, D2, and TRβ2 mRNA expression, which (with the exception of TSHβ) can be prevented by leptin administration during fasting. Following 24 h fasting, 4 h refeeding completely restores pituitary D2 and TRβ2 mRNA expression, while a single leptin dose is ineffective. This indicates that other postingestion signals may be necessary to modulate rapidly the fasting-induced decrease in pituitary D2 and TRβ2 mRNA expression.

scholarly journals Interleukin-1β modulates endogenous thyroid hormone receptor α gene transcription in liver cells

2007 ◽  
Vol 194 (2) ◽  
pp. 257-265 ◽  
Author(s):  
J Kwakkel ◽  
W M Wiersinga ◽  
A Boelen
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Gene Transcription ◽  
Hormone Receptor ◽  
Proinflammatory Cytokine ◽  
Hepg2 Cells ◽  
Promoter Activity ◽  
Thyroid Hormone Receptor ◽  
De Novo ◽  
Hepatoma Cells

One of the main characteristics of nonthyroidal illness (NTI) is a decrease in serum triiodothyronine, partly caused by a decrease in liver deiodinase type 1 (D1) mRNA and activity. Proinflammatory cytokines have been associated with NTI in view of their capability to decrease D1 and thyroid hormone receptor (TR)β1 mRNA expression in hepatoma cells. Proinflammatory cytokine induction leads to activation of the inflammatory pathways nuclear factor (NF)κB and activator protein (AP)-1. The proinflammatory cytokine interleukin (IL)-1β decreases thyroid hormone receptor (TR)β1 mRNA in an NFκB-dependent way. The aim of this study was to unravel the effects of IL-1β on endogenous TRα gene expression in an animal model and in a liver cell line. The TRα gene product is alternatively spliced in TRα1 and TRα2, TRα2 is capable of inhibiting TRα1-induced gene transcription. We showed that both TRα1 and TRα2 mRNA decreased not only after lipopolysaccharide administration in liver of mice, but also after IL-1β stimulation of hepatoma cells (HepG2). Using the NFκB inhibitor sulfasalazine and the AP-1 inhibitor SP600125, it became clear that the IL-1β-induced decrease in TRα mRNA expression in HepG2 cells can only be abolished by simultaneous inhibition of NFκB and AP-1. The IL-1β-induced TRα1 and TRα2 mRNA decrease in HepG2 cells is the result of decreased TRα gene promoter activity, as evident from actinomycin D experiments. Cycloheximide experiments showed that the decreased promoter activity is independent of de novo protein synthesis and therefore most likely due to posttranslational modifications such as phosphorylation or subcellular relocalization.

Retinoid-Related Receptor (ROR) α mRNA Expression Is Altered in the Brain of Male Mice Lacking All Ligand-Binding Thyroid Hormone Receptor (TR) Isoforms

Endocrine ◽  
2005 ◽  
Vol 26 (1) ◽  
pp. 025-032 ◽  
Author(s):  
Nandini Vasudevan ◽  
Hosein Kami Kia ◽  
Maria Hadjimarkou ◽  
Noriyuki Koibuchi ◽  
William W. Chin ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Ligand Binding ◽  
Mrna Expression ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Male Mice ◽  
The Brain

The Thyroid Hormone Receptor (TR) β-Selective Agonist GC-1 Inhibits Proliferation But Induces Differentiation and TR β mRNA Expression in Mouse and Rat Osteoblast-Like Cells

2009 ◽  
Vol 84 (4) ◽  
pp. 324-333 ◽  
Author(s):  
Eduardo H. Beber ◽  
Luciane P. Capelo ◽  
Tatiana L. Fonseca ◽  
Cristiane C. Costa ◽  
Claudimara F. Lotfi ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Mrna Expression ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Selective Agonist ◽  
Rat Osteoblast
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