Hormone-Dependent Regulation of Intercellular Adhesion Molecule-1 Gene Expression: Cloning and Analysis of 5′-Regulatory Region of Rat Intercellular Adhesion Molecule-1 Gene in FRTL-5 Rat Thyroid Cells

Thyroid ◽  
1999 ◽  
Vol 9 (6) ◽  
pp. 601-612 ◽  
Author(s):  
EUN SHIN PARK ◽  
SOON HEE YOU ◽  
HO KIM ◽  
O-YU KWON ◽  
HEUNG KYU RO ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adhesion Molecule ◽  
Regulatory Region ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Expression Cloning ◽  
Intercellular Adhesion Molecule 1 ◽  
Thyroid Cells ◽  
Rat Thyroid

Adhesion molecule expression by the FRTL-5 rat thyroid cell line

1991 ◽  
Vol 130 (3) ◽  
pp. 451-456 ◽  
Author(s):  
N. Tandon ◽  
C. Dinsdale ◽  
T. Tamatani ◽  
M. Miyasaka ◽  
A. P. Weetman
Keyword(s):  
Cell Line ◽  
Adhesion Molecule ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Thyroid Cell ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Thyroid Cells ◽  
Thyroid Cell Line ◽  
Rat Thyroid

ABSTRACT We have examined the expression and function of rat CD54, a homologue of human intercellular adhesion molecule-1 (ICAM-1), by the continuously growing rat thyroid cell line FRTL-5. Approximately 10% of FRTL-5 cells express CD54 under basal conditions and this is not influenced by thyrotrophin. Expression of CD54 is increased by cytokines (γ-interferon, tumour necrosis factor, interleukin-1) and by an activator of C-kinase, phorbol 12-myristate 13-acetate. Blocking ICAM-1 with a monoclonal antibody directed against this molecule significantly (P <0·01) reduced the binding of splenic lymphocytes to FRTL-5 cells but inhibition was consistently greater (P <0·01) in the presence of antibodies against a rat homologue of lymphocyte function-associated antigen-1, the receptor on T cells for ICAM-1. In no case was complete blocking of cluster formation observed. These results show that a pure line of rat thyroid cells can express an ICAM-1 homologue and this is directly enhanced by cytokines. Expression of this homologue is partially responsible for lymphocyte adhesion to thyroid cells, which is likely to be a major event in T cell recognition of thyroid antigens in autoimmune thyroiditis. Journal of Endocrinology (1991) 130, 451–456

Expression of membrane and soluble intercellular adhesion molecule-1 in Graves' disease

1997 ◽  
Vol 19 (2) ◽  
pp. 191-201 ◽  
Author(s):  
C Massart ◽  
E Sonnet ◽  
J Gibassier ◽  
N Genetet ◽  
G Leclech ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Adhesion Molecule ◽  
Calf Serum ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Human Thyroid ◽  
Graves Disease ◽  
Intercellular Adhesion Molecule 1 ◽  
Thyroid Cells ◽  
Soluble Intercellular Adhesion Molecule

We have investigated the in vitro expression of membrane and soluble intercellular adhesion molecule-1 (ICAM-1) by human thyroid cells from 20 patients with Graves' disease and 5 normal subjects. Membrane ICAM-1 was not detected by flow cytometry analysis in non-cultured thyrocytes from either normal or Graves' disease tissues. It appeared on thyroid cells after a 24-h culture in monolayers and showed a regular dose-dependent increase. The same results were obtained with soluble ICAM-1 (sICAM-1) in culture media from cells cultured in monolayers, vesicles or follicles. No change was obtained with different concentrations of fetal calf serum added to the media. Coculture of Graves' disease thyrocytes with autologous peripheral blood lymphocytes (PBL) or intrathyroidal lymphocytes (ITL) enhanced the expression of both membrane and sICAM-1 whatever the culture model. When normal thyrocytes were cocultured with PBL, sICAM-1 increased but with ITL sICAM-1 remained unchanged. High concentrations of gamma interferon induced an increase of both membrane and sICAM-1 in the three culture models. However the increases were greater with vesicles and follicles. Only sICAM-1 levels were raised with 0.1, 1 and 10 microM retinoic acid. These results suggest that ICAM-1 appears in culture, possibly due to mechanical effects such as adherence to plates and cell-to-cell contacts. Moreover, its expression is modulated by several factors such as cytokines or retinoic acid. Further investigations are needed to establish whether ICAM-1 is really involved in the pathogenesis of Graves' disease.

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