Studies of the histogenesis of the thyroid gland of the guinea pig. I. The thyroid cells (follicle cells and parafollicular cells)

1954 ◽  
Vol 120 (2) ◽  
pp. 363-377 ◽  
Author(s):  
Shooichi Sugiyama
1967 ◽  
Vol 37 (2) ◽  
pp. 205-NP ◽  
Author(s):  
G. BUSSOLATI ◽  
A. G. E. PEARSE

SUMMARY In the pig, the C cells of the thyroid gland, which are the counterparts of parafollicular cells of Nonidez in the thyroid of the dog, are mainly epifollicular rather than parafollicular. Using guinea-pig anti-pig calcitonin, and an indirect ('sandwich') technique, immunofluorescence tests indicated that calcitonin in the pig thyroid is present in cells which are morphologically indistinguishable from the C cells. Calcitonin was also present in cells which resemble pericytes. Taking advantage of cross-reactivity between canine calcitonin and anti-pig calcitonin antibody, a similar localization (C cells and pericytes) could be shown by immunofluorescence tests in the thyroid of dogs. These results confirm previous work indicating that the parafollicular cells are responsible for the production and secretion of thyrocalcitonin. The role of the pericytes has not been established with certainty.


1971 ◽  
Vol 12 (4) ◽  
pp. 560-571
Author(s):  
L.-A. Lindberg ◽  
S. Talanti

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.


1973 ◽  
Vol 11 (3) ◽  
pp. 9-10

Calcitonin is a polypeptide hormone secreted by the parafollicular cells of the thyroid gland in mammals. It inhibits bone resorption and lowers both serum and urinary calcium concentrations. Human calcitonin is available only in very small quantities but has been used in some studies. The first commercially available preparation in Britain is a porcine calcitonin (Calcitare - Armour).


1999 ◽  
Vol 112 (9) ◽  
pp. 1405-1416
Author(s):  
D. Claisse ◽  
I. Martiny ◽  
B. Chaqour ◽  
Y. Wegrowski ◽  
E. Petitfrere ◽  
...  

Transforming growth factor beta1 (TGF-beta1) is a secreted polypeptide that is thought to play a major role in the regulation of folliculogenesis and differentiation of thyroid cells. On porcine thyroid follicular cells cultured on plastic substratum, TGF-beta1, in a concentration-dependent way, promoted the disruption of follicles, cell spreading, migration and confluency by a mechanism that did not involve cell proliferation. TGF-beta1 strongly activated the production of thrombospondin-1 and (alpha)vbeta3 integrin in a concentration-dependent manner whereas the expression of thyroglobulin was unaffected. Anisomycin, an inhibitor of protein synthesis, inhibited the effect of TGF-beta1 on cell organization. Thrombospondin-1 reproduced the effect of TGF-beta1. In the presence of thrombospondin-1 cells did not organize in follicle-like structures but, in contrast, spreaded and reached confluency independently of cell proliferation. This effect is suppressed by an RGD-containing peptide. The adhesive properties of thrombospondin-1 for thyroid cells were shown to be mediated by both the amino-terminal heparin-binding domain and the RGD domain of thrombospondin-1. Adhesion was shown to involve (alpha)vbeta3 integrin. The results show that TGF-beta1 exerted an influence upon function and behaviour of follicle cells partly mediated by the synthesis of thrombospondin-1 and of its receptor (alpha)vbeta3 integrin.


Author(s):  
Ildiko Lingvay ◽  
Shelby A. Holt

The thyroid gland, which is the largest endocrine organ, secretes primarily thyroid hormones that play a critical role in the normal growth and development of the maturing human. In the adult, thyroid hormones maintain metabolic stability by regulating oxygen requirements, body weight, and intermediary metabolism. Thyroid function is under hypothalamic-pituitary control, and thus, like the gonads and adrenal cortex, it serves as a classical model of endocrine physiology. In addition, the physiological effects of thyroid hormones are regulated by complex extrathyroidal mechanisms resulting from the peripheral metabolism of the hormones, mechanisms that are not under hypothalamic-pituitary regulation. Thyroid function abnormalities are very prevalent, especially in females and in certain geographic areas, and are often a result of autoimmunity or iodine deficiency. The thyroid originates from two distinct parts of the embryonic endoderm: • The follicular structures arise from a midline thickening of the anterior pharyngeal floor (the base of the tongue), adjacent to the differentiating heart. This thyroid diverticulum first expands ventrally while still attached to the pharyngeal floor by its stalk (thyroglossal duct), and then expands laterally, leading to the characteristic bilobed structure. As the developing heart descends, the thyroid gets pulled into its final position, a process that leads to the rapid stretch and degeneration of the thyroglossal duct. • The parafollicular cells are derived from the ultimobranchial bodies (originating from the neural crest) but ultimately are surrounded by the medial thyroid. The parafollicular cells represents <10 % of the adult thyroid gland. The thyroid completes its structural development by 9 weeks of gestation, the first endocrine organ to assume its definitive form during organogenesis; yet full functional maturation and integration with the hypothalamic-pituitary axis continues throughout gestation. Abnormal thyroid development can lead to persistence of the thyroglossal duct, presence of ectopic thyroid tissue (lingual thyroid, lateral aberrant thyroid), and malposition (thoracic goiter), all of which can remain clinically silent or present later in life as diagnostic challenges. The shape of the human thyroid resembles that of a butterfly.


1975 ◽  
Vol 142 (4) ◽  
pp. 485-497 ◽  
Author(s):  
Nancy McNamara ◽  
Virginia H. Black
Keyword(s):  

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