Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

Roger, Pierre P.; Dumont, Jacques Emile

doi:10.1016/0303-7207(84)90087-x

Cited by 199 publications

(93 citation statements)

References 40 publications

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“…Many studies indicate that TSH has TGA (Drexhage et al, 1980;Valente et al, 1983b;Roger and Dumont, 1984;Stringer et al, 1985;Dere and Rapoport, 1986 ;Jin et al, 1986;Ealey et al, 1987Tramontano et al, 1988Zakarija and Mckenzie, 1989), including [3H] Tdr incorporation in FRTL-5 cells as a convenient and reproducible index (Valente et al, 1983a;Jin et al, 1986;Tramontano et al, 1988;Zakarija and Mckenzie, 1989). In the present study, we showed that not only TSH but also hCG has TGA by measuring [3H] Tdr incorporation in FRTL-5 cells, which is consistent with other reports (Davies and Platzer, 1986;Hershman et al, 1988).…”

Section: Discussionsupporting

confidence: 92%

Human Chorionic Gonadotropin Promotes Thyroid Growth via Thyrotropin Receptors in FRTL-5 Cells.

et al. 1990

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Section: Discussionsupporting

confidence: 92%

Human Chorionic Gonadotropin Promotes Thyroid Growth via Thyrotropin Receptors in FRTL-5 Cells.

et al. 1990

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“…TSH induces human thyroid cell growth at a higher concentration than is necessary for induction of differentiated function (39).…”

Section: Iodine Intake and Thyroid Cancermentioning

confidence: 99%

“…Iodine deficient thyroid cells will have an increased content of the two major intracellular messengers for the TSH signaling pathways, cAMP and Ca ++ (39). Under this condition, the thyroid cell is sensitized to TSH stimulation, which elicit responses that are inappropriately high for a given stimulation.…”

Section: Increased Thyroid Cell Responsiveness To Tshmentioning

confidence: 99%

Relevance of iodine intake as a reputed predisposing factor for thyroid cancer

Knobel

Medeiros‐Neto

2007

Arq Bras Endocrinol Metab

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Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of TSH. This may be associated to thyroid cancer risk, particularly in women. Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals. Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFβ 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China. In conclusion: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.

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“…In primary cultures, the effects of FGF on thyroid cells appear inconsistent but this may be related to regulation of receptor expression. An initial report of studies with dog thyroid cells showed mitogenic (Roger & Dumont 1984) and dedifferentiating effects (Gerard et al 1989), while studies using human thyroid cells found no effect on growth (Taylor et al 1993). FGFs are not normally secreted in free form, and their effectiveness as mitogens is dependent upon release from the extracellular matrix.…”

Section: Fgfs and Fgf Receptorsmentioning

confidence: 99%

Growth factors and goitrogenesis

Bidey¹,

Hill²,

Eggo³

1999

Journal of Endocrinology

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By combining data from studies of multinodular non-toxic goitre (MNTG) with data from rat models of goitre induction and in vitro models, a map of the growth factors involved in goitrogenesis has been constructed. We have addressed the roles of the insulin-like growth factors, transforming growth factors, fibroblast growth factors, endothelins, etc. We hypothesise that an imbalance in the interactions between the various growth factor axes exists in MNTG which favours cell replication. Thyrotrophin, although not significantly elevated in MNTG, exerts critical effects through interactions with autocrine and paracrine factors and their receptors. Expansion of the thyroidal vascular bed through angiogenesis is closely co-ordinated with follicular cell expansion and folliculoneogenesis, and while the integrated paracrine actions of fibroblast growth factors, vascular endothelial growth factor and endothelin probably play central roles, additional, as yet elusive, factors are probably involved. The combination of in vitro and in vivo approaches, designed to address specific questions, will undoubtedly continue to prove invaluable in dissecting further the complex interactions that exist between these growth factors, their binding proteins and receptors in goitrogenesis.

show abstract

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

Cited by 199 publications

References 40 publications

Human Chorionic Gonadotropin Promotes Thyroid Growth via Thyrotropin Receptors in FRTL-5 Cells.

Human Chorionic Gonadotropin Promotes Thyroid Growth via Thyrotropin Receptors in FRTL-5 Cells.

Relevance of iodine intake as a reputed predisposing factor for thyroid cancer

Growth factors and goitrogenesis

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