scholarly journals A PURE STRAIN OF THYROID CELLS AND ITS CHARACTERISTICS

1925 ◽  
Vol 41 (3) ◽  
pp. 337-346 ◽  
Author(s):  
Albert H. Ebeling

1. A pure strain of thyroid epithelium was isolated and maintained in active condition for 7 months. At the end of the experiment, the rate of cell multiplication was as great as at its beginning. 2. The thyroid cells grew at the surface of the coagulum as pavement epithelium, and within the coagulum as a glandular structure. 3. The cells did not dedifferentiate, and the lumen of the acini in cultures from a strain over 4 months old contained colloid secretion similar morphologically to that from a freshly extirpated thyroid gland.

2003 ◽  
Vol 51 (4) ◽  
pp. 479-483 ◽  
Author(s):  
Svetlana B. Savin ◽  
Dubravka S. Cvejić ◽  
Miroslava M. Janković

High levels of expression of galectin-1 and galectin-3, the β-galactoside-binding proteins, have been recently described in malignant thyroid tumors but not in adenomas nor in normal thyroid tissue. However, there are no data about the expression of these galectins during fetal thyroid development. In this study we analyzed immunohistochemically the presence of galectin-1 and galectin-3 in human fetal thyroid glands (16–37 weeks of gestation). Weak to moderate cytoplasmic staining for galectin-1 was observed in follicular cells of all fetal thyroids. Galectin-3 could not be detected in thyroid follicular cells of any fetal thyroid investigated. Both galectins were detected in stromal tissue, but staining for galectin-1 was more intense. The absence of galectin-3 in thyroid cells during fetal development suggests that galectin-3 is expressed de novo during malignant transformation of thyroid epithelium, and that galectin-1 could be considered an oncofetal antigen. The results obtained indicated potential roles for galectin-1 and galectin-3 during the investigated period of human fetal thyroid gland development. Both galectins might participate in developmental processes regarding stromal fetal thyroid tissue organization, whereas galectin-1 might have a function in thyroid epithelium maturation.


2021 ◽  
Author(s):  
Ekaterina Timokhina ◽  
◽  
Nataliya Yaglova ◽  
Sergey Obernikhin ◽  
Valentin Yaglov ◽  
...  

Dynamics of morphological changes in the thyroid gland of mice, consuming water with lower deuterium content, was studied. Primary changes in structure were indicative of more active hormone secretion. Later morphological signs of inhibited hormone secretion were found. The findings demonstrate sensitivity of thyroid cells to shifts in deuterium body con-tent.


1990 ◽  
Vol 189 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Osamu Tachiwaki ◽  
Joseph D. Zeligs ◽  
Seymour H. Wollman

1937 ◽  
Vol 66 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Harald Okkels

1. During the 1st and 2nd day of cultivation of the whole thyroid gland in the Lindbergh apparatus, perfused by a medium containing 20 or 40 per cent homologous serum diluted with glucose-Tyrode, the state of the thyroid epithelium remains histologically normal and even the most delicate cytological details retain their normal aspect. 2. Cultivation over a period up to 6 days need not cause any serious histological alteration of the gland; but cytological examination reveals an increasingly damaged condition of the mitochondria and the Golgi apparatus. These changes seem not to interfere with the life of the cells, however; epithelial culture from the perfused organs yields positive results. 3. The process of cultivation is liable to cause a slight morphological reaction in the thyroid epithelium, which resembles a feeble stimulation of the tissue. 4. Addition of the thyro-stimulating factor from the anterior pituitary to the perfusion fluid causes a stimulation of the cultivated thyroid epithelium which is comparable to, but not so marked as, the corresponding reaction in the living animal.


2008 ◽  
Vol 294 (2) ◽  
pp. E291-E299 ◽  
Author(s):  
Gaëlle Prost ◽  
Françoise Bernier-Valentin ◽  
Yvonne Munari-Silem ◽  
Samia Selmi-Ruby ◽  
Bernard Rousset

Thyroid epithelial cells communicate through gap junctions formed from connexin (Cx)32, Cx43, and Cx26. We previously reported that reexpression of Cx32 in “gap junction-deficient” FRTL-5 and FRT thyroid cell lines induces a reduction of cell proliferation rate and an activation of expression of cell differentiation. The present study aimed at determining whether Cx32 could exert similar regulatory functions in vivo. We investigated morphological and functional characteristics of thyroid gland of Cx32-deficient mice (Cx32-KO), mice overexpressing Cx32 selectively in the thyroid (Cx32-T+), and Cx32-KO mice with a thyroid-selective Cx32 complementation obtained by crossing Cx32-KO and Cx32-T+ mice. In basal conditions, Cx32-KO mice did not present any detectable thyroid alteration, whereas Cx32-T+ mice showed a thyroid hypoplasia (20% reduction) associated with a slight increase in thyroid functional activity. Under thyrotropin stimulation (following sodium perchlorate treatment), Cx32-KO mice developed a larger goiter (≤65% increase) than wild-type littermates, whereas Cx32-T+ mice exhibited the same thyroid hyperplasia as wild-type mice. Restoration of Cx32 expression in the thyroid of Cx32-KO mice abrogated the thyroid growth increase related to Cx32 deficiency. All together, these data show that Cx32 acts as a downregulator of growth of thyroid gland; an excess of Cx32 limits growth of thyroid cells in the basal state, whereas a lack of Cx32 confers an additional growth potential to TSH-stimulated thyroid cells.


2014 ◽  
Vol 83 (2) ◽  
pp. 167-172
Author(s):  
Małgorzata Włochal ◽  
Marcin A. Kucharski ◽  
Marian Grzymisławski

Hashimoto’s thyroiditis (HT), also known as chronic lymphocytic thyroiditis is one of the most frequent types of inflammation of the thyroid gland. The prevalence of the overt HT is about 2% but it is believed that Hashimoto thyroiditis is more frequent than expected. Hashimoto’s thyroiditis is characterized by dysfunction of the immune system, which leads to impaired tolerance of own tissues and increased production of autoantibodies against the thyroid cells. Thyroid peroxidase antibodies (anti-TPO), thyroglobulin antibodies (anti-Tg) and/or TSH receptors antibodies are the principal markers of the disease. The essential element of the treatment of HT is the supplementation of L-thyroxine. In Hashimoto’s disease, like in many other autoimmune diseases, researchers attempted to support pharmacological treatment by adequate nutrition. The aim of this paper was to review the existing literature on the levels of antioxidants (vitamin A, C, E, selenium, zinc) and vitamin D in patients with HT, as well as the influence of the nutritional supplementation of the above mentioned elements on the metabolism of the thyroid gland hormones and the level of anti-thyroid peroxidase (anti-TPO) antibodies.


2021 ◽  
Vol 27 (1) ◽  
pp. 66-71
Author(s):  
O.V. Fedosieieva ◽  
O.I. Pototska

In clinical practice, synthetic glucocorticoids, such as dexamethasone, are used to accelerate fetal maturation in pregnant women at risk of preterm birth. Increasing the concentration of cortisol in humans and other mammals often causes structural and functional changes in fetal tissues, preparing it for childbirth and extrauterine life, but they can have long-term consequences in the structural organization of organs postnatally. Despite the large number of studies on the effect of glucocorticoids on the fetus, there are almost no data on the prenatal effect of dexamethasone on the processes of synthesis and resorption of thyroglobulin by thyroid thyrocytes in the postnatal period of life. Therefore, the aim of the study was to determine the immunohistochemical features of expression and distribution of antibodies to thyroglobulin in the thyroid glands of newborn rats in normal and after prenatal exposure to dexamethasone. The study material was the thyroid gland of Wistar rats aged 1 to 7 days of postnatal development (54 animals): I group - intact animals (norm); ІІ group - control, animals which were injected with 0.9% NaCl solution at a dose of 0.05 ml to each fetus on the 18th day of dated pregnancy; III group - experimental animals, which were administered a solution of dexamethasone at a dilution of 1:40 at a dose of 0.05 ml to each fetus on the 18th day of the date of pregnancy operatively during laparotomy, by intrauterine, transdermal subcutaneous injection into the interscapular area (Ukrainian patent №112288). Thyroglobulin Antibody (2H11) monoclonal antibodies: sc-51708 from Santa Cruz Biotechnology, Inc. were used for immunohistochemical study. Photo documentation of the studied objects was performed using a “Primo Star” microscope (Carl Zeiss, Germany) using an AxioCam camera using the Zeiss Zen program (2011). Analysis of micropreparations of thyroid glands of intact and control rats showed invariance of thyroglobulin synthesis and its accumulation, which was expressed by sufficient immunohistochemical expression of antibodies to thyroglobulin (ТgAb+). Prenatal administration of dexamethasone leads to intensification of the processes of morphological development of hormone-producing structures (follicles and follicular epithelium), production, resorption and iodination of thyroglobulin. This is evidenced by immunohistochemical studies found in 1-3 days of the neonatal period. It should be noted that on the 7th day of life the newborn was found intense changes in the structure of the parenchyma of the thyroid gland of animals of the experimental group: increased relative percentage of follicle cavity due to increased number of large and medium, some follicles had no resorption vacuoles which was accompanied by a slowdown in the excretion of hormones into the bloodstream and led to overstretching of the follicles and, as a consequence, to the flattening of the thyroid epithelium. Intrauterine administration of dexamethasone leads to prenatal acceleration of structure formation, folliculogenesis and enhancement of hormone-producing function, which is confirmed by the peculiarities of immunohistochemical expression of TgAb. By the end of the neonatal period in rats prenatally exposed to dexamethasone, the thyroid gland is depleted of compensatory-reactive internal reserves, which is morphologically and immunohistochemically manifested by signs of hypofunction and hypertrophy. Thus, detected in the thyroid glands of animals prenatally exposed to dexamethasone, aberration of cytoplasmic expression of ТgAb+, intensification of colloidal expression of ТgAb+, flattening of thyroid epithelium, and the absence of resorption vacuoles are signs of impaired hormone-forming function, which is the morphological basis for the development of hypofunctional states and requires further study.


1993 ◽  
Vol 264 (4) ◽  
pp. E644-E649
Author(s):  
A. S. Yap ◽  
J. W. Armstrong ◽  
E. J. Cragoe ◽  
J. R. Bourke ◽  
G. J. Huxham ◽  
...  

The thyroid epithelium possesses a bidirectional fluid transport system capable of absorbing Na+ and secreting Cl-. In the present studies we have examined its possible role in the regulation of thyroid follicular size. When exposed to hypotonic media (200 mosM) cultured porcine thyroid follicles first swelled and then displayed a regulatory volume decrease (RVD) over 60 min. This was associated with a transient depolarization of the transepithelial potential difference (TEP) and subsequent hyperpolarization with a time course similar to RVD. Phenamil (1 microM), an antagonist of epithelial Na+ channels, did not affect initial swelling but prevented the subsequent follicular RVD. Phenamil abolished hyperpolarization of TEP, but the loop diuretic bumetanide, which inhibits Cl- secretion in thyroid cells, did not prevent it. Exposure to hypotonic medium produced a slow hyperpolarization of the intracellular potential (basolateral membrane potential) consistent with an increase in basolateral membrane K+ conductance. Ba2+ and quinidine, which are known to inhibit K+ channels in epithelia, prevented RVD. Addition of the K+ ionophore valinomycin (1 microM) caused follicle shrinkage that was prevented by phenamil (1 microM). We conclude that cultured follicles respond to hypotonically induced stretch by activating outwardly directed Na+ transport through a mechanism which involves change in the basolateral K+ conductance. This response would be characteristic of a system that controlled follicle volume. However, it is not clear from these studies whether the cells responded primarily to the increase in follicle volume or to the change in cell volume that is expected to accompany hypotonic challenge.


Development ◽  
1966 ◽  
Vol 16 (3) ◽  
pp. 487-496
Author(s):  
Harold Fox

In a previous work on pronephric degeneration, larvae of Rana temporaria from practically the whole range of the metamorphic cycle were studied (Fox, 1962). Metamorphosis in anurans is dependent upon the presence of a functional thyroid gland (Kollros, 1951; Lynn & Wachowski, 1951; Etkin, 1964), and the same specimens have now been used to investigate thyroid growth and development quantitatively and qualitatively, especially in relation to those major events which occur at the metamorphic climax between stages 49 and 54 (Cambar & Marrot, 1954). It will be shown that in larvae from 16 mm long (stage 41; see Fox, 1962) until practically the end of the climax (stage > 53), thyroid cells are of stable volume (about 700 μ3), and thyroid enlargement is by cellular proliferation and vesicular expansion. The maximum rate of thyroid growth occurs between 16 mm and 28 mm (stages 41–45).


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