scholarly journals Single strand DNA-binding proteins and thyroid transcription factor-1 conjointly regulate thyrotropin receptor gene expression.

1995 ◽  
Vol 9 (5) ◽  
pp. 527-539
Author(s):  
H Shimura ◽  
Y Shimura ◽  
M Ohmori ◽  
S Ikuyama ◽  
L D Kohn
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Dna Binding ◽  
Receptor Gene ◽  
Dna Binding Proteins ◽  
Thyrotropin Receptor ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Transcription Factor 1 ◽  
Receptor Gene Expression

scholarly journals Modulation of Thyroid-Specific Gene Expression in Normal and Nodular Human Thyroid Tissues from Adults: An in Vivo Effect of Thyrotropin

2005 ◽  
Vol 90 (10) ◽  
pp. 5692-5697 ◽  
Author(s):  
Rocco Bruno ◽  
Elisabetta Ferretti ◽  
Emanuele Tosi ◽  
Franco Arturi ◽  
Paolo Giannasio ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Human Thyroid ◽  
Normal Tissues ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Group 2 ◽  
Transcription Factor 1 ◽  
Tsh Levels

Context: Evidence from in vitro studies or animal models has shown that TSH affects thyrocytes by thyroid-specific expression modulation. Objective: The objective of our study was to analyze the role of TSH in human thyroid gene expression in vivo. Design/Setting: Thirty-nine normal thyroid tissues were collected at the same center. Study Subjects: Patients were divided into two groups based on serum TSH levels: 17 with normal TSH levels (1–4 mU/liter; group 1) and 22 with TSH levels below 0.5 mU/liter (group 2). Intervention: Group 2 underwent thyroidectomy after suppressive l-T4 therapy. Main Outcome Measures: mRNA levels of thyroid genes such as sodium/iodide symporter (NIS), apical iodide transporter, pendrin, thyroglobulin, thyroperoxidase, TSH receptor, paired box transcription factor 8, and thyroid transcription factor-1 were evaluated by quantitative PCR. Results: The reduction of TSH stimulation causes decreases in NIS and apical iodide transporter gene expression in normal tissues and more limited reductions in thyroglobulin, thyroperoxidase, and paired box transcription factor 8, but it has no significant effect on TSH receptor, pendrin, or thyroid transcription factor-1. Comparison of NIS levels in normal and nodular tissues from the same patient confirmed that it is differentially expressed in nodules only in the presence of normal TSH (P < 0.01). In patients with suppressed TSH, nodular NIS levels were similar to those in normal tissues. Conclusions: Our data represent the first demonstration in human thyroid tissues that TSH contributes to the regulation of thyrocyte differentiation by modulating thyroid gene levels. It exerts a particularly important effect on the transcription of NIS, which becomes very low after prolonged TSH suppression.

Sign in / Sign up

Export Citation Format

Share Document