Hormonal regulation of ICAM-1 gene expression in thyroid cells, FRTL-5.
- Author:
Bong Soo AN
1
;
Bon Jeong KU
;
So Young PARK
;
Jae Kyu SHIN
;
Jin Hong LEE
;
Young Kun KIM
;
Min Ho SHONG
;
Heung Kyu RO
Author Information
1. CHUNGNAM NATL UNIV, SCH MED, DEPT INTERNAL MED, TAEJON 301040, SOUTH KOREA.
- Publication Type:Original Article
- Keywords:
thyrotropin;
cAMP;
rat ICAM-1;
thyroid;
FRTL-5;
cytokines
- MeSH:
Animals;
Clone Cells;
Cloning, Organism;
Colforsin;
Cytokines;
Gene Expression*;
Graves Disease;
Humans;
Hydrocortisone;
Insulin;
Intercellular Adhesion Molecule-1*;
Interferon-gamma;
Interleukin-1beta;
Interleukin-6;
Necrosis;
Rats;
RNA, Messenger;
Self Tolerance;
Thyroid Gland*;
Thyrotropin;
Tumor Necrosis Factor-alpha
- From:Experimental & Molecular Medicine
1997;29(1):45-51
- CountryRepublic of Korea
- Language:English
-
Abstract:
Our previous works have shown that human thyroid follicular cells from Graves' disease and FRTL-5 rat thyroid cells express the intercellular adhesion molecule-1 (ICAM-1) molecule and its expression is upregulated by several cytokines, interferon-gamma, tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6. We used FRTL-5 cells which show hormonal dependence of growth and function for the study of hormonal regulation of ICAM-1 gene, We studied ICAM-1 mRNA expression and promoter regulation after cloning of rat ICAM-1 promoter. We found very interesting findings that thyroid stimulating hormone (TSH) and forskolin downregulates steady state MHC class land ICAM-1 mRNA levels in FRTL-5 cells; furthermore, TSH/cAMP inhibit cytokines (interferon-gamma,tumor necrosis factor-alpha)-mediated maximal ICAM-1 mRNA expression, In addition, hydrocortisone and insulin differentially regulate the ICAM-1 mRNA levels; hydrocortisone markedly suppresses the mRNA level but insulin partially recovers hydrocortisone mediated ICAM-1 suppression, The interferon-gamma and tumor necrosis factor-alpha increases full ICAM-1 promoter (pCAM-1822) activity and this cytokine mediated increase of the promoter activity is also inhibited by TSH and forskolin, Thus TSH/cAMP pathways play roles as a antagonistic action for maximal expression of ICAM-1 gene by these cytokines. We propose this TSH action is one of physiologic mechanisms to preserve self tolerance in face of abnormal cytokine challenges in systemic inflammatory condition or acute phase response.
