Regulation of Inhibitors of Differentiation Family Proteins by Thyroid-Stimulating Hormone in FRTL-5 Thyroid Cells.
10.3346/jkms.2008.23.2.262
- Author:
Young Suk JO
1
;
Eun Suk HWANG
;
Ju Hee LEE
;
Yunhyeong LEE
;
Seul Young KIM
;
Yun Sun CHOI
;
Youn Sun BAI
;
Jun Hwa HONG
;
Yun Jeung KIM
;
Ihn Suk LEE
;
So Young RHA
;
Heung Kyu RO
;
Minho SHONG
Author Information
1. Division of Endocrinology, Department of Internal Medicine, Eulji University School of Medicine, Daejeon, Korea.
- Publication Type:Original Article
- Keywords:
Thyroid Gland;
Thyrotropin;
Id2 protein
- MeSH:
1-Phosphatidylinositol 3-Kinase/metabolism;
Animals;
Cattle;
Cell Differentiation;
Cell Proliferation;
*Gene Expression Regulation;
Inhibitor of Differentiation Protein 2/metabolism;
Insulin/metabolism;
Paired Box Transcription Factors/metabolism;
Promoter Regions, Genetic;
Proto-Oncogene Proteins c-myc/metabolism;
Rats;
Thyroglobulin/metabolism;
Thyroid Gland/*cytology;
Thyrotropin/*metabolism
- From:Journal of Korean Medical Science
2008;23(2):262-269
- CountryRepublic of Korea
- Language:English
-
Abstract:
Members of the inhibitors of differentiation (Id) family of helix-loop-helix (HLH) proteins are known to play important roles in the proliferation and differentiation of many cell types. Thyroid-stimulating hormone (TSH) regulates proliferation and differentiation by activating TSH receptor (TSHR) in thyrocytes. In this study, we found that Id2, one of the Id family proteins, is a major target for regulation by TSH in FRTL-5 thyroid cells. TSH rapidly increases the Id2 mRNA level in FRTL-5 thyroid cells but the Id2 protein showed biphasic regulatory patterns, being transiently reduced and subsequently induced by TSH treatment. Transient reduction of Id2 protein was noted within 2 hr of TSH treatment and was mediated by proteasomal degradation. Moreover, reduced Id2 expression correlated with the activity of the phosphatidylinositol 3 kinase pathway, which is activated by TSH. Although TSH increases the activity of the Id2 promoter, TSH-induced activation of this promoter was independent of c-Myc. Id2 did not alter TTF-1- and Pax-8-mediated effects on the regulation of the Tg promoter. Thus, in summary, we found that TSH regulates Id2 expression, but that Id2 does not alter the expression of thyroid-specific genes, such as Tg, in FRTL-5 thyroid cells.
