Studies on the mechanism of desensitization of the cyclic amp response to tsh stimulation in a cloned rat thyroid cell line

1985 ◽  
Vol 42 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Hideshi Hirayu ◽  
Ronald P. Magnusson ◽  
Basil Rapoport
1987 ◽  
Vol 247 (3) ◽  
pp. 519-524 ◽  
Author(s):  
J B Field ◽  
P A Ealey ◽  
N J Marshall ◽  
S Cockcroft

Studies were conducted to determine whether thyroid-stimulating hormone (TSH; thyrotropin), a hormone known to increase cytosol concentrations of cyclic AMP, also stimulates the formation of inositol phosphates in thyroid cells. TSH and noradrenaline both stimulated [3H]inositol phosphate formation in a concentration-dependent manner in the rat thyroid cell line, FRTL-5 cells, which had been prelabelled with [3H]inositol. The threshold concentration of TSH required to stimulate inositol phosphate formation was more than 20 munits/ml, which is approx. 10(3)-fold greater than that required for cyclic AMP accumulation and growth in these cells. We also demonstrate that membranes prepared from FRTL-5 cells possess a guanine nucleotide-activatable polyphosphoinositide phosphodiesterase, which suggests that activation of inositide metabolism in these cells may be coupled to receptors by the G-protein, Gp. Our findings suggest that two second-messenger systems exist to mediate the action of TSH in the thyroid.


1987 ◽  
Vol 115 (3) ◽  
pp. 481-487 ◽  
Author(s):  
A. P. Weetman ◽  
C. Green ◽  
L. K. Borysiewicz

ABSTRACT We have used the continuously growing FRTL-5 rat thyroid cell line to examine the regulation of major histocompatibility complex (MHC) class II (or la) antigen expression. Of the various stimuli investigated, only the supernatant from activated T cells or recombinant γ-interferon induced Ia expression. All Ia-inducing activity was removed from the T cell supernatant by acid dialysis, suggesting that γ-interferon is the single critical mediator for class II antigen expression. Its action was not TSH dependent but expression of class II antigens increased from the G0-G1 to the S and G2 phases of the cell cycle, so that TSH enhanced Ia expression by its action on cell division. Other agents including lectins, hormones, epidermal growth factor, a calcium ionophore and a phorbol ester did not induce Ia expression. Substances known to inhibit murine macrophage Ia expression (cortisol, prostaglandin E2 and 5-hydroxytryptamine) had no effect on FRTL-5 Ia expression. The use of this thyroid cell line has permitted direct examination of modulators in the absence of any possible effects from contaminating non-thyroid cells present in primary cultures and the results suggest that, of the agents tested, only γ-interferon has significance in the context of Ia antigen expression by the thyroid. J. Endocr. (1987) 115, 481–487


1991 ◽  
Vol 130 (3) ◽  
pp. 451-456 ◽  
Author(s):  
N. Tandon ◽  
C. Dinsdale ◽  
T. Tamatani ◽  
M. Miyasaka ◽  
A. P. Weetman

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


2010 ◽  
Vol 42 (12) ◽  
pp. 897-899 ◽  
Author(s):  
A. Klagge ◽  
K. Krause ◽  
K. Müller ◽  
J. Haag ◽  
D. Fuhrer

1990 ◽  
Vol 122 (4) ◽  
pp. 520-526 ◽  
Author(s):  
Å. Krogh Rasmussen ◽  
L. Kayser ◽  
K. Bech ◽  
U. Feldt-Rasmussen ◽  
H. Perrild ◽  
...  

Abstract The effects of human recombinant interleukin 1α (20 pg/1-2 μg/l) and 1β (200 pg/1-20 μg/l) on two systems of thyroid cells have been compared. The thyroglobulin and cAMP secretion and the DNA content of human thyroid cells cultured in monolayer and of continuously grown rat thyroid cells, Fischer rat thyroid cell line have been studied. The growth of the rat thyroid cell line was inhibited by interleukin 1β (20 ng/1-20 μg/l), but not by interleukin 1α. None of the cytokines changed the cAMP production of the rat thyroid cells. In contrast, both cAMP production and thyroglobulin secretion were inhibited dose-dependently by the cytokines in human thyroid cells in secondary cultures. These results caution the interpretation and extrapolation of changes induced by interleukin 1 from one cell system to the other.


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