Recombinant γ-interferon stimulates iodide uptake and cyclic AMP production by the FTRL5 thyroid cell line

FEBS Letters ◽  
1987 ◽  
Vol 221 (1) ◽  
pp. 91-94 ◽  
Author(s):  
A.P. Weetman
Keyword(s):  
Cyclic Amp ◽  
Cell Line ◽  
Thyroid Cell ◽  
Iodide Uptake ◽  
Thyroid Cell Line ◽  
Γ Interferon

Regulation of major histocompatibility complex class II antigen expression by the FRTL-5 rat thyroid cell line

1987 ◽  
Vol 115 (3) ◽  
pp. 481-487 ◽  
Author(s):  
A. P. Weetman ◽  
C. Green ◽  
L. K. Borysiewicz
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Line ◽  
Antigen Expression ◽  
Class Ii ◽  
Thyroid Cell ◽  
Histocompatibility Complex ◽  
Thyroid Cell Line ◽  
Rat Thyroid ◽  
Class Ii Antigen ◽  
Γ Interferon

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

Immune induction of major histocompatibility complex antigens on a human thyroid cell line (SGHTL-34)

1989 ◽  
Vol 2 (3) ◽  
pp. 183-187 ◽  
Author(s):  
S. L. King ◽  
G. St J. Whitley ◽  
S. Page ◽  
S. S. Nussey ◽  
A. P. Johnstone
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Line ◽  
Class Ii ◽  
Class I ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Histocompatibility Complex ◽  
Thyroid Cell Line ◽  
Class Ii Antigens ◽  
Γ Interferon

ABSTRACT Expression of major histocompatibility complex antigens by epithelial cells may play a role in the aetiology of autoimmune disorders. We have studied the effect of γ-interferon on SGHTL-34, a human thyroid cell line which constitutively expresses class I but not class II antigens. γ-Interferon induced the expression of class II and increased the expression of class I molecules (assessed by flow cytofluorimetry) in a dose-dependent manner. Thyrotrophin or phytohaemagglutinin had no effect on either class I or class II expression. However, a supernatant from phytohaemagglutinin-stimulated peripheral blood mononuclear cells, containing 6400 U γ-interferon/ml, was an effective inducer of both class I and class II antigens. These data clarify earlier studies using primary thyroid cultures, which are contaminated with cells of the immune system.

scholarly journals TSH-induced cyclic AMP production in an ovine thyroid cell line: OVNIS 5H

FEBS Letters ◽  
1986 ◽  
Vol 194 (2) ◽  
pp. 287-291 ◽  
Author(s):  
Guy Fayet ◽  
Azédine Aouani ◽  
Sonia Hovsépian
Keyword(s):  
Cyclic Amp ◽  
Cell Line ◽  
Thyroid Cell ◽  
Thyroid Cell Line

scholarly journals Thyroid-stimulating hormone stimulates increases in inositol phosphates as well as cyclic AMP in the FRTL-5 rat thyroid cell line

1987 ◽  
Vol 247 (3) ◽  
pp. 519-524 ◽  
Author(s):  
J B Field ◽  
P A Ealey ◽  
N J Marshall ◽  
S Cockcroft
Keyword(s):  
Cyclic Amp ◽  
Cell Line ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Cell ◽  
Dependent Manner ◽  
Thyroid Cell Line ◽  
Rat Thyroid ◽  
Stimulating Hormone

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.

scholarly journals MTOR downregulates iodide uptake in thyrocytes

2010 ◽  
Vol 206 (1) ◽  
pp. 113-120 ◽  
Author(s):  
Elaine Cristina Lima de Souza ◽  
Álvaro Souto Padrón ◽  
William Miranda Oliveira Braga ◽  
Bruno Moulin de Andrade ◽  
Mário Vaisman ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Line ◽  
Thyroid Cell ◽  
Synthetic Analog ◽  
Iodide Uptake ◽  
Mtor Inhibition ◽  
Thyroid Cell Line ◽  
Pi3k Inhibition ◽  
Rat Thyroid

Phosphoinositide-3-kinase (PI3K) inhibition increases functional sodium iodide symporter (NIS) expression in both FRTL-5 rat thyroid cell line and papillary thyroid cancer lineages. In several cell types, the stimulation of PI3K results in downstream activation of the mechanistic target of rapamycin (MTOR), a serine–threonine protein kinase that is a critical regulator of cellular metabolism, growth, and proliferation. MTOR activation is involved in the regulation of thyrocyte proliferation by TSH. Here, we show that MTOR inhibition by rapamycin increases iodide uptake in TSH-stimulated PCCL3 thyroid cell line, although the effect of rapamycin was less pronounced than PI3K inhibition. Thus, NIS inhibitory pathways stimulated by PI3K might also involve the activation of proteins other than MTOR. Insulin downregulates iodide uptake and NIS protein expression even in the presence of TSH, and both effects are counterbalanced by MTOR inhibition. NIS protein expression levels were correlated with iodide uptake ability, except in cells treated with TSH in the absence of insulin, in which rapamycin significantly increased iodide uptake, while NIS protein levels remained unchanged. Rapamycin avoids the activation of both p70 S6 and AKT kinases by TSH, suggesting the involvement of MTORC1 and MTORC2 in TSH effect. A synthetic analog of rapamycin (everolimus), which is clinically used as an anticancer agent, was able to increase rat thyroid iodide uptake in vivo. In conclusion, we show that MTOR kinase participates in the control of thyroid iodide uptake, demonstrating that MTOR not only regulates cell survival, but also normal thyroid cell function both in vitro and in vivo.

Cellular damage in vitro

2009 ◽  
Vol 48 (05) ◽  
pp. 208-214 ◽  
Author(s):  
J. Drechsel ◽  
R. Freudenberg ◽  
R. Runge ◽  
G. Wunderlich ◽  
J. Kotzerke ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Survival ◽  
Cell Line ◽  
Cellular Damage ◽  
Thyroid Cell ◽  
Response Curves ◽  
Beta Emitters ◽  
Thyroid Cell Line ◽  
Clonogenic Cell ◽  
Radionuclide Uptake

Summary Aim: The cellular damage of ionising radiation depends on dose, physical radiation quality (e. g. LET) and intracellular radionuclide uptake. The influence of two beta emitters (188Re and 131I) on the thyroid cell line PC Cl3 was studied. Furthermore, we analysed the effect of intracellular accumulation. Methods: The thyroid cell line PC Cl3 was irradiated with 188Re-perrhenate or 131I-sodium iodide in presence or absence of perchlorate. The initial DNA-damage was measured in the comet assay as olive tail moment (OTM). The colony forming assay detects the clonogenic cell survival as surviving fraction. Additional the intracellular radionuclide uptake was quantified. Results: Dose response curves were established for irradiation with 188Re-perrhenate or 131I-iodine under various extra- and intracellular activity distribution conditions. In the presence of perchlorate DNA-damage and clonogenic cell survival for both radionuclides were comparable. In the absence of perchlorat radionuclide uptake of 1.39% (131I) and 4.14% (188Re) were measured causing twofold higher radiotoxicity. Although 131I uptake was lower than 188Re uptake the OTM values were higher und surviving fractions were lower. Conclusions: 131I, compared to 188Re, has lower mean beta energy and a higher LET, and therefore, it induced a higher DNA-damage even at lower intracellular uptake. An additional explanation for the higher radiotoxicity of 131I could be the higher dose exposition caused by crossfire through neighborhood cells.

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