scholarly journals Potential role of two novel agonists of thyroid hormone receptor‐β on liver regeneration

2020 ◽  
Vol 53 (5) ◽  
Author(s):  
Andrea Perra ◽  
Marta Anna Kowalik ◽  
Lavinia Cabras ◽  
Massimiliano Runfola ◽  
Simona Sestito ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Liver Regeneration ◽  
Hormone Receptor ◽  
Potential Role ◽  
Thyroid Hormone Receptor ◽  
Thyroid Hormone Receptor Β

Potential role of two novel agonists of thyroid hormone receptor-beta on liver regeneration

2020 ◽  
Vol 73 ◽  
pp. S249
Author(s):  
Andrea Perra ◽  
Marta Anna Kowalik ◽  
Lavinia Cabras ◽  
Simona Onali ◽  
Cristina Migliore ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Liver Regeneration ◽  
Hormone Receptor ◽  
Potential Role ◽  
Thyroid Hormone Receptor ◽  
Receptor Beta

scholarly journals Lacking thyroid hormone receptor β gene does not influence alterations in peripheral thyroid hormone metabolism during acute illness

2008 ◽  
Vol 197 (1) ◽  
pp. 151-158 ◽  
Author(s):  
J Kwakkel ◽  
O Chassande ◽  
H C van Beeren ◽  
W M Wiersinga ◽  
A Boelen
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Males And Females ◽  
Induced Changes ◽  
Thyroid Hormone Receptor Β

The downregulation of liver deiodinase type 1 (D1) is supposed to be one of the mechanisms behind the decrease in serum tri-iodothyronine (T3) observed during non-thyroidal illness (NTI). Liver D1 mRNA expression is positively regulated by T3, mainly via the thyroid hormone receptor (TR)β1. One might thus expect that lacking the TRβ gene would result in diminished downregulation of liver D1 expression and a smaller decrease in serum T3 during illness. In this study, we used TRβ−/− mice to evaluate the role of TRβ in lipopolysaccharide (LPS, a bacterial endotoxin)-induced changes in thyroid hormone metabolism. Our results show that the LPS-induced serum T3 and thyroxine and liver D1 decrease takes place despite the absence of TRβ. Furthermore, we observed basal differences in liver D1 mRNA and activity between TRβ−/− and wild-type mice and TRβ−/− males and females, which did not result in differences in serum T3. Serum T3 decreased rapidly after LPS administration, followed by decreased liver D1, indicating that the contribution of liver D1 during NTI may be limited with respect to decreased serum T3 levels. Muscle D2 mRNA did not compensate for the low basal liver D1 observed in TRβ−/− mice and increased in response to LPS in TRβ−/− and WT mice. Other (TRβ independent) mechanisms like decreased thyroidal secretion and decreased binding to thyroid hormone-binding proteins probably play a role in the early decrease in serum T3 observed in this study.

scholarly journals Thyroid Hormone Resistance in the Heart: Role of the Thyroid Hormone Receptor β Isoform

Endocrinology ◽  
2004 ◽  
Vol 145 (4) ◽  
pp. 1625-1633 ◽  
Author(s):  
Tania M. Ortiga-Carvalho ◽  
Koshi Hashimoto ◽  
Carmen C. Pazos-Moura ◽  
David Geenen ◽  
Ronald Cohen ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Hormone Resistance ◽  
Thyroid Hormone Resistance ◽  
Thyroid Hormone Receptor Β

scholarly journals Thyroid hormone receptor β mutations in the ‘hot-spot region’ are rare events in thyroid carcinomas

2007 ◽  
Vol 192 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Ana Sofia Rocha ◽  
Ricardo Marques ◽  
Inês Bento ◽  
Ricardo Soares ◽  
João Magalhães ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Hormone ◽  
Transgenic Mice ◽  
Cell Lines ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Hot Spot ◽  
Direct Sequencing ◽  
Human Thyroid ◽  
Thyroid Hormone Receptor Β

Thyroid cancer constitutes the most frequent endocrine neoplasia. Targeted expression of rearranged during transfection (RET)/papillary thyroid carcinoma (PTC) and V600E V-raf murine sarcoma viral oncogene homolog B1 (BRAF) to the thyroid glands of transgenic mice results in tumours similar to those of human PTC, providing evidence for the involvement of these oncogenes in PTC. Kato et al. developed a mouse model that mimics the full spectrum of the human follicular form of thyroid cancer (FTC). FTC rapidly develops in these mice through introduction of the thyroid hormone receptor β (THRB)PV mutant on the background of the inactivated THRB wt locus. Our aim was to verify if, in the context of human follicular thyroid carcinogenesis, THRB acted as a tumour suppressor gene. We screened for mutations of the THRB gene in the hot-spot region, spanning exons 7–10, in 51 thyroid tumours and six thyroid cancer cell lines by PCR and direct sequencing. We did not find mutations in any of the tumours or cell lines analysed. Our findings suggest that, in contrast to the findings on the THRB-mutant transgenic mice, THRB gene mutations are not a relevant mechanism for human thyroid carcinogenesis.

A Novel Point Mutation of Thyroid Hormone Receptor β Gene in a Family with Resistance to Thyroid Hormone

Thyroid ◽  
1997 ◽  
Vol 7 (5) ◽  
pp. 771-773 ◽  
Author(s):  
TOMOHISA NAGASHIMA ◽  
HIDEKI YAGI ◽  
KANJI NAGASHIMA ◽  
AKIHIRO SAKURAI ◽  
KAZUMICHI ONIGATA ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Point Mutation ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Resistance To Thyroid Hormone ◽  
Thyroid Hormone Receptor Β

scholarly journals Oncogenic mutations of thyroid hormone receptor β

Oncotarget ◽  
2015 ◽  
Vol 6 (10) ◽  
pp. 8115-8131 ◽  
Author(s):  
Jeong Won Park ◽  
Li Zhao ◽  
Mark Willingham ◽  
Sheue-yann Cheng
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Oncogenic Mutations ◽  
Thyroid Hormone Receptor Β
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