Autonomous Growth and Function of Cultured Thyroid Follicles from Cats with Spontaneous Hyperthyroidism

Peter, H J; Gerber, H; Studer, H; Peterson, Mark E.; Becker, David V.; Groscurth, Peter

doi:10.1089/thy.1991.1.331

Cited by 32 publications

(32 citation statements)

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“…Similar to findings with human TNG, xenotransplantation of feline hyperthyroid tissue into athymic mice showed continued growth and function of the transplanted tissue, even with suppression of TSH secretion in the host (15). Furthermore, cultured feline hyperthyroid cell follicles imbedded in collagen to preserve their three-dimensional structure showed TSH-independent increases in radiolabeling with 3 H thymidine and 131 I-Na (20). Taken together, these data suggest that, similar to TNG, feline hyperthyroidism is an autonomous disease caused by cellular abnormalities, resulting in constitutively active cells that are TSH-independent.…”

Section: Introductionsupporting

confidence: 70%

Thyrotropin-Stimulated DNA Synthesis and Thyroglobulin Expression in Normal and Hyperthyroid Feline Thyrocytes in Monolayer Culture

Ward

Achenbach

Holt

et al. 2005

Thyroid

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Feline hyperthyroidism is a common, spontaneous disease in older cats that is similar clinically and histopathologically to human toxic multinodular goiter (TNG). In this study, the functional response of feline normal thyroid (NT) and hyperthyroid (HT) cells grown in monolayer culture to thyrotropin (TSH) was determined. Basal levels of DNA synthesis were similar in NT and HT cells. TSH stimulated concentration-dependent DNA synthesis in NT and HT cells, with maximal stimulation seen at 1 and 10 mU/mL TSH in NT and HT cells, respectively. HT cells had higher basal levels of thyroglobulin (Tg) expression. TSH stimulated Tg expression in NT and HT cells in a concentration-dependent fashion, with maximal activity at 0.5 and 5 mU/mL TSH, respectively. These results demonstrate that NT and HT cells in monolayer culture exhibit growth and functional responses to TSH. HT cells have higher basal Tg expression than NT cells and require higher TSH concentrations to stimulate DNA synthesis and Tg expression, two measures of thyroid cell activation. These data support the idea that feline hyperthyroidism is caused by cell abnormalities, resulting in dysregulated growth and hormone synthesis, and emphasize its importance as an animal model for TNG.

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Section: Introductionsupporting

confidence: 70%

Thyrotropin-Stimulated DNA Synthesis and Thyroglobulin Expression in Normal and Hyperthyroid Feline Thyrocytes in Monolayer Culture

Ward

Achenbach

Holt

et al. 2005

Thyroid

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“…Studies using primary cultures of follicles and thyrocytes from toxic adenomatous cat thyroids Consistent with these xenotransplantation studies, adenomatous thyroid cells from hyperthyroid cats cultured in TSH-free media also continue to grow and function autonomously (Peter et al 1991). In those studies, primary cultures of enzymatically dissociated follicles from 15 hyperthyroid cat goiters and from three normal cat thyroid glands were embedded in collagen gels to preserve their 3D structure.…”

mentioning

confidence: 74%

“…6). Similarly, twice as many follicular cells of hyperfunctioning thyroid tissue, maintained without TSH in the medium, were labeled after exposure to 3 H-thymidine than in follicles from normal glands (Peter et al 1991;Fig. 7).…”

mentioning

confidence: 91%

“…TSH stimulated mitogenesis and thyroglobulin expression in both normal and hyperthyroid cells, but a higher concentration of TSH was needed to maximally stimulate both activities in the hyperthyroid cells (Ward et al 2005a). Other studies of monolayer hyperthyroid cell culture, however, found no effect of TSH on 3 H-thymidine uptake in hyperthyroid cells (Gerber et al 1991), illustrating that cells from different feline goiters may show a high degree of heterogeneity in culture. Overall, these data reinforce the idea that feline toxic nodular goiter cells have a high level of basal, unstimulated activity with dysregulated growth and hormone synthesis, as would be expected in autonomous cells (Gerber et al 1994, Ward et al 2005a).…”

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confidence: 91%

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ANIMAL MODELS OF DISEASE: Feline hyperthyroidism: an animal model for toxic nodular goiter

Peterson¹

2014

Journal of Endocrinology

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“…Cats are the only other mammalian species in which spontaneous thyrotoxicosis occurs frequently [112]. The pathogenic mechanisms underlying feline hyperthyroidism remain controversial, as both an autonomous mechanism of growth and function, and an autoimmune etiology have been proposed [112,113]. However, a recent study, using cells transfected with the feline TSH receptor, provides further evidence against the presence of TSH receptor antibodies in hyperthyroid cats [30].…”

Section: Animal Models For Graves' Diseasementioning

confidence: 99%

Human Genome and Diseases: Review¶The TSH receptor and its role in thyroid disease

Kopp

2001

CMLS, Cell. Mol. Life Sci.

122

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The thyrotropin (TSH) receptor plays a preeminent role in thyroid physiology and disease. TSH, acting through the TSH receptor, is the major stimulator of thyroid cell growth, differentiation and function. In Graves' disease, the TSH receptor is the target of stimulating antibodies that cause hyperthyroidism. Although still a topic of debate, the TSH receptor has been implicated in the pathogenesis of the endocrine ophthalmopathy associated with Graves' disease. Blocking antibodies against the TSH receptor are involved in the development of hypothyroidism in a subset of patients with autoimmune hypothyroidism. Transplacental passage of stimulating or blocking TSH receptor antibodies from a mother with autoimmune thyroid disease may result in transient hyper- or hypothyroidism in early infancy. During pregnancy, the placental hormone human choriogonadotropin (hCG) can cause gestational hyperthyroidism through cross-reaction with the TSH receptor. Gestational hyperthyroidism may also be involved in the pathogenesis of hyperemesis gravidarum. Trophoblast tumors secreting hCG are a rare cause of hyperthyroidism. Somatic activating mutations of the TSH receptor have been identified as a molecular cause of toxic adenomas, whereas activating mutations in the germline give rise to nonautoimmune familial hyperthyroidism or sporadic congenital hyperthyroidism. These gain-of-function mutations are dominant, and one mutated allele is sufficient to result in disease. Inactivating germline mutations of both TSH receptor alleles lead to variable degrees of resistance to TSH, encompassing a spectrum ranging from euthyroid hyperthyrotropinemia to overt hypothyroidism with thyroid hypoplasia.

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Autonomous Growth and Function of Cultured Thyroid Follicles from Cats with Spontaneous Hyperthyroidism

Cited by 32 publications

References 11 publications

Thyrotropin-Stimulated DNA Synthesis and Thyroglobulin Expression in Normal and Hyperthyroid Feline Thyrocytes in Monolayer Culture

Thyrotropin-Stimulated DNA Synthesis and Thyroglobulin Expression in Normal and Hyperthyroid Feline Thyrocytes in Monolayer Culture

ANIMAL MODELS OF DISEASE: Feline hyperthyroidism: an animal model for toxic nodular goiter

Human Genome and Diseases: Review¶The TSH receptor and its role in thyroid disease

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