Interleukin-1 receptors on human thyroid cells and on the rat thyroid cell line FRTL-5

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

Journal of Endocrinology ◽

10.1677/joe.0.1300451 ◽

1991 ◽

Vol 130 (3) ◽

pp. 451-456 ◽

Cited By ~ 13

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

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CALCITRIOL ATTENUATES IODIDE UPTAKE IN A RAT THYROID CELL LINE

Vitamin D ◽

10.1515/9783110850345-123 ◽

1991 ◽

pp. 401-402

Keyword(s):

Cell Line ◽

Thyroid Cell ◽

Iodide Uptake ◽

Thyroid Cell Line ◽

Rat Thyroid

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Trace Amine-Associated Receptor 1 Trafficking to Cilia of Thyroid Epithelial Cells

Cells ◽

10.3390/cells10061518 ◽

2021 ◽

Vol 10 (6) ◽

pp. 1518

Author(s):

Maria Qatato ◽

Vaishnavi Venugopalan ◽

Alaa Al-Hashimi ◽

Maren Rehders ◽

Aaron D. Valentine ◽

...

Keyword(s):

Cell Surface ◽

Cell Lines ◽

Human Thyroid ◽

Apical Plasma Membrane ◽

Thyroid Cell ◽

Thyroid Cells ◽

Trace Amine ◽

Rat Thyroid

Trace amine-associated receptor 1 (rodent Taar1/human TAAR1) is a G protein-coupled receptor that is mainly recognized for its functions in neuromodulation. Previous in vitro studies suggested that Taar1 may signal from intracellular compartments. However, we have shown Taar1 to localize apically and on ciliary extensions in rodent thyrocytes, suggesting that at least in the thyroid, Taar1 may signal from the cilia at the apical plasma membrane domain of thyrocytes in situ, where it is exposed to the content of the follicle lumen containing putative Taar1 ligands. This study was designed to explore mouse Taar1 (mTaar1) trafficking, heterologously expressed in human and rat thyroid cell lines in order to establish an in vitro system in which Taar1 signaling from the cell surface can be studied in future. The results showed that chimeric mTaar1-EGFP traffics to the apical cell surface and localizes particularly to spherical structures of polarized thyroid cells, procilia, and primary cilia upon serum-starvation. Moreover, mTaar1-EGFP appears to form high molecular mass forms, possibly homodimers and tetramers, in stably expressing human thyroid cell lines. However, only monomeric mTaar1-EGFP was cell surface biotinylated in polarized human thyrocytes. In polarized rat thyrocytes, mTaar1-EGFP is retained in the endoplasmic reticulum, while cilia were reached by mTaar1-EGFP transiently co-expressed in combination with an HA-tagged construct of the related mTaar5. We conclude that Taar1 trafficking to cilia depends on their integrity. The results further suggest that an in vitro cell model was established that recapitulates Taar1 trafficking in thyrocytes in situ, in principle, and will enable studying Taar1 signaling in future, thus extending our general understanding of its potential significance for thyroid autoregulation.

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Cloning the Fisher Rat Thyroid Cell Line (FRTL-5): Variability in Clonal Growth and 3′5′-Cyclic Adenosine Monophosphate Response to Thyrotropin*

Endocrinology ◽

10.1210/endo-121-1-78 ◽

1987 ◽

Vol 121 (1) ◽

pp. 78-83 ◽

Cited By ~ 24

Author(s):

TERRY F. DAVIES ◽

CLEMENT YANG ◽

MICHAEL PLATZER

Keyword(s):

Cell Line ◽

Clonal Growth ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Thyroid Cell ◽

Thyroid Cell Line ◽

Rat Thyroid

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

Journal of Endocrinology ◽

10.1677/joe.0.1150481 ◽

1987 ◽

Vol 115 (3) ◽

pp. 481-487 ◽

Cited By ~ 7

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

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Acrylamide does not induce tumorigenesis or major defects in mice in vivo

Journal of Endocrinology ◽

10.1677/joe-08-0123 ◽

2008 ◽

Vol 198 (2) ◽

pp. 301-307 ◽

Cited By ~ 4

Author(s):

Ling Jin ◽

Vanessa Chico-Galdo ◽

Claude Massart ◽

Christine Gervy ◽

Viviane De Maertelaere ◽

...

Keyword(s):

Thyroid Hormone ◽

Chronic Administration ◽

Serum Levels ◽

Human Thyroid ◽

Thyroid Cell ◽

Thyroid Cells ◽

Hormone Synthesis ◽

Rat Thyroid

Chronic administration of acrylamide has been shown to induce thyroid tumors in rat. In vitro acrylamide also causes DNA damage, as demonstrated by the comet assay, in various types of cells including human thyroid cells and lymphocytes, as well as rat thyroid cell lines. In this work, mice were administered acrylamide in their drinking water in doses comparable with those used in rats, i.e., around 3–4 mg/kg per day for mice treated 2, 6, and 8 months. Some of the mice were also treated with thyroxine (T4) to depress the activity of the thyroid. Others were treated with methimazole that inhibits thyroid hormone synthesis and consequently secretion and thus induces TSH secretion and thyroid activation. These moderate treatments were shown to have their known effect on the thyroid (e.g. thyroid hormone and thyrotropin serum levels, thyroid gland morphology…). Besides, T4 induced an important polydipsia and degenerative hypertrophy of adrenal medulla. Acrylamide exerted various discrete effects and at high doses caused peripheral neuropathy, as demonstrated by hind-leg paralysis. However, it did not induce thyroid tumorigenesis. These results show that the thyroid tumorigenic effects of acrylamide are not observed in another rodent species, the mouse, and suggest the necessity of an epidemiological study in human to conclude on a public health policy.

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