In vitro and in vivo regulation of thyrotropin receptor mRNA levels in dog and human thyroid cells.

Although primary cultures of human thyroid cells are used for endocrinological and toxicological studies, until now no attention has been paid toward verifying whether the hormonal conditions to which the gland was exposed in vivo prior to surgery could influence in vitro responses. Our findings suggest that the hormonal situation in vivo cannot be used as a predictive indicator of triiodothyronine and thyroxine release and/or S-phase frequency in vitro, either with or without the addition of bovine thyrotropin.

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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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Sensitization and desensitization of human thyroid cells in culture: effects of thyrotrophin and thyroid-stimulating immunoglobulin

Journal of Endocrinology ◽

10.1677/joe.0.1190341 ◽

1988 ◽

Vol 119 (2) ◽

pp. 341-349 ◽

Cited By ~ 8

Author(s):

Z. Kraiem ◽

R. Alkobi ◽

O. Sadeh

Keyword(s):

Secretory Activity ◽

Time Lapse ◽

Human Thyroid ◽

Thyroid Cells ◽

Subsequent Exposure ◽

Heterologous Desensitization ◽

High Doses ◽

Culture Effects

ABSTRACT Using an in-vitro system of cultured human thyroid cells and cyclic AMP (cAMP) accumulation as an index of cell stimulation, we compared TSH and thyroid-stimulating immunoglobulin (TSI) with regard to thyrocyte sensitization and desensitization. The smallest dose of TSH (0·05 mU/ml) capable of stimulating thyroid cells was the same as the minimum dose required to induce desensitization upon subsequent rechallenge with the hormone. In contrast, about 30-fold higher doses of TSI were needed to cause cell refractoriness compared with doses capable of eliciting stimulation. Moreover, significant stimulation of the thyroid with TSI was apparent much later than with TSH. A longer time-lapse was also necessary for TSI to induce densensitization. Likewise, thyrocytes recovered more slowly from TSI compared with TSH desensitization. Although at high doses TSI induced homologous desensitization, at lower doses the antibody, unlike TSH, potentiated the cAMP response to subsequent exposure to the antibody. The stimulatory doses of TSI were in the range usually encountered in active Graves' disease, which may explain why prolonged TSI in vivo sustains a hyperthyroid condition. In addition, we found that under conditions in which TSH leads to desensitization of the cAMP response, the thyroid cells maintained their responsiveness in terms of triiodothyronine secretory activity. Pre-exposure of human thyrocytes to TSI induced heterologous desensitization towards the TSH-stimulated cAMP response. Moreover, addition of the antibody to maximally desensitizing doses of TSH decreased cell sensitivity to the hormone even further. In sharp contrast, preincubation of cells with TSH, or TSH plus TSI, potentiated by four- and twofold respectively the cAMP response to subsequent challenge with TSI. Taken together, the data reveal marked differences between the action of TSH and TSI, and raise interesting questions concerning the mechanism whereby TSH potentiates the cAMP response to TSI. J. Endocr. (1988) 119, 341–349

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Differential regulation of thyrotropin-releasing hormone receptor mRNA levels by thyroid hormone in vivo and in vitro (GH3 cells)

Biochemical and Biophysical Research Communications ◽

10.1016/0006-291x(92)91202-2 ◽

1992 ◽

Vol 184 (1) ◽

pp. 367-372 ◽

Cited By ~ 29

Author(s):

Masanobu Yamada ◽

Tuyoshi Monden ◽

Teturou Satoh ◽

Masahiko Iizuka ◽

Masami Murakami ◽

...

Keyword(s):

Thyroid Hormone ◽

Hormone Receptor ◽

Differential Regulation ◽

Thyrotropin Releasing Hormone ◽

Gh3 Cells ◽

Mrna Levels ◽

Releasing Hormone ◽

Receptor Mrna

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IN-VITRO STUDIES OF NORMAL HUMAN THYROID CELLS: RESPONSES TO THYROTROPHIN AND DIBUTYRYL CYCLIC AMP

Journal of Endocrinology ◽

10.1677/joe.0.0720087 ◽

1977 ◽

Vol 72 (1) ◽

pp. 87-96 ◽

Cited By ~ 12

Author(s):

S. P. BIDEY ◽

P. MARSDEN ◽

J. ANDERSON ◽

C. G. McKERRON ◽

H. BERRY

Keyword(s):

Cyclic Amp ◽

Thyroid Tissue ◽

Three Dimensional ◽

Human Thyroid ◽

Dibutyryl Cyclic Amp ◽

Iodide Uptake ◽

Thyroid Cells ◽

Normal Human

SUMMARY Follicular cells isolated from normal human thyroid tissue have been cultured for up to 140 h with bovine thyrotrophin (TSH) or dibutyryl cyclic AMP (DBcAMP). Both compounds induced marked reorganization of the cells into three-dimensional follicular structures, whilst non-supplemented cells assumed a monolayer form. Cultures treated initially with TSH or DBcAMP showed a greater iodide uptake capacity, in comparison with unsupplemented cultures, in which iodide uptake was markedly diminished after 24 h. The release of tri-iodothyronine (T3) and thyroxine (T4) into the medium was determined by radioimmunoassay. Both TSH- and DBcAMP-treated cells showed a significant increase in iodothyronine output compared with unsupplemented control cells. In contrast to the 'classical' TSH-induced depression of the T4:T3 ratio in vivo, an increase in the ratio was observed for both TSH- and DBcAMP-supplemented cells in vitro. The ratio was also significantly greater after TSH than after DBcAMP, and possible implications of this finding are discussed.

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Reexpression of blood group ABH antigens on the surface of human thyroid cells in culture.

The Journal of Cell Biology ◽

10.1083/jcb.94.1.193 ◽

1982 ◽

Vol 94 (1) ◽

pp. 193-200 ◽

Cited By ~ 5

Author(s):

E L Khoury

Keyword(s):

Cell Surface ◽

Blood Group ◽

Enzymatic Digestion ◽

Cell Suspensions ◽

Human Thyroid ◽

Blood Group Antigens ◽

Thyroid Cells ◽

Blood Group Abh

Using indirect immunofluorescence (IFL) on viable human thyroid cultures, it has been shown that, although adult follicular cells do not express blood group ABH antigens in vivo, they invariably reexpress the corresponding antigens on the cell surface when cultured in monolayers, even for very short periods. The absence of blood group antigens on noncultured thyroid cells was confirmed by negative IFL on cell suspensions obtained after enzymatic digestion of the glands, whereas these antigens were readily demonstrable on cell suspensions obtained by trypsinization of established monolayers. The quantitative expression of ABH antigens on individual thyroid cells was variable and the cell-surface IFL pattern due to binding of blood group isoantibodies was different from that given by organ-specific thyroid autoantibodies on viable cultures. Reexpression of blood group antigens by cultured thyroid cells could not be related to the secretor status of the donors, the presence of a particular source of serum in the culture medium or cell division in vitro. After 2-3 wk in culture, thyroid cells became morphologically dedifferentiated and no longer displayed blood group antigens, though they still expressed cell-surface beta 2-microglobulin. Fibroblasts present in the primary thyroid cultures were invariably negative for ABH antigens. These results demonstrate that the surface antigenic repertoire of cultured human cells is not necessarily identical to that present on the same cells in vivo. Furthermore, the possibility that blood group natural isoantibodies bind to the cell surface must be taken into account in experiments in which cultured thyroid cells are exposed to human sera.

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Transforming acidic coiled-coil 3 and Aurora-A interact in human thyrocytes and their expression is deregulated in thyroid cancer tissues

Endocrine Related Cancer ◽

10.1677/erc-07-0053 ◽

2007 ◽

Vol 14 (3) ◽

pp. 827-837 ◽

Cited By ~ 33

Author(s):

Salvatore Ulisse ◽

Enke Baldini ◽

Matteo Toller ◽

Jean-Guy Delcros ◽

Aurélie Guého ◽

...

Keyword(s):

Cell Cycle ◽

Thyroid Cancer ◽

Coiled Coil ◽

Human Thyroid ◽

Mrna Levels ◽

Aurora A Kinase ◽

Aurora A ◽

Thyroid Cells ◽

Cancer Tissues

Aurora-A kinase has recently been shown to be deregulated in thyroid cancer cells and tissues. Among the Aurora-A substrates identified, transforming acidic coiled-coil (TACC3), a member of the TACC family, plays an important role in cell cycle progression and alterations of its expression occur in different cancer tissues. In this study, we demonstrated the expression of the TACC3 gene in normal human thyroid cells (HTU5), and its modulation at both mRNA and protein levels during cell cycle. Its expression was found, with respect to HTU5 cells, unchanged in cells derived from a benign thyroid follicular tumor (HTU42), and significantly reduced in cell lines derived from follicular (FTC-133), papillary (B-CPAP), and anaplastic thyroid carcinomas (CAL-62 and 8305C). Moreover, in 16 differentiated thyroid cancer tissues, TACC3 mRNA levels were found, with respect to normal matched tissues, reduced by twofold in 56% of cases and increased by twofold in 44% of cases. In the same tissues, a correlation between the expression of the TACC3 and Aurora-A mRNAs was observed. TACC3 and Aurora-A interact in vivo in thyroid cells and both proteins localized onto the mitotic structure of thyroid cells. Finally, TACC3 localization on spindle microtubule was no more observed following the inhibition of Aurora kinase activity by VX-680. We propose that Aurora-A and TACC3 interaction is important to control the mitotic spindle organization required for proper chromosome segregation.

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