Thyroid Hormone Action: A Cell-Culture System Responsive to Physiological Concentrations of Thyroid Hormones

Samuels, Herbert H.; Tsai, Jir S.; Cintron, Raquel

doi:10.1126/science.181.4106.1253

Cited by 184 publications

(76 citation statements)

References 26 publications

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“…Pituitary cell lines are typically responsive to thyroid hormone given the high TR expression in the gland (101). The GH1 somatotroph cell line was among the first cell models shown to respond to physiological levels of thyroid hormone as monitored by cell growth and glucose utilization (531). In the GH3 somatotroph cell line, exposure to T 3 increases growth hormone expression in a TRb2-mediated manner (532), while in GH-secreting GC cells, T 3 decreases D2 mRNA levels (143).…”

Section: Bianco Et Almentioning

confidence: 99%

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Bianco

Anderson

Forrest

et al. 2014

Thyroid

175

106

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Section: Bianco Et Almentioning

confidence: 99%

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Bianco

Anderson

Forrest

et al. 2014

Thyroid

175

106

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“…In the various growth hormone-producing rat pituitary tumor cell lines (GH cells) for example, T3 is the most potent thyroid hormone analogue in stimulating glucose consumption (2), growth hormone production (3), and amino acid transport (4), and these effects correlate well with the proportion of nuclear binding sites occupied by T3. Although 3,3',5Y-triiodothyronine (rT3) also has agonist activity in GH cells, 1,000-fold greater concentrations are required, presumably due to the nuclear receptor having a significantly lower affinity for rT3 (5).…”

Section: Introductionmentioning

confidence: 99%

Metabolic effect of 3,3',5'-triiodothyronine in cultured growth hormone-producing rat pituitary tumor cells. Evidence for a unique mechanism of thyroid hormone action.

Germain¹

1985

J. Clin. Invest.

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Physiologic levels of 3,3',5'-triiodothyronine (rT3) are generally believed to have minimal metabolic effects in the pituitary gland and other tissues. In the present studies, the regulatory role of rT3 and other thyroid hormones on iodothyronine 5'-deiodinase (15D) activity was studied in a growth hormoneproducing rat pituitary tumor cell line (GH3 cells). O5D activity was thiol-dependent and displayed nonlinear reaction kinetics suggesting the presence of two enzymatic processes, one having a low Michaelis constant (K. for thyroxine IT41 of 2 nM) and a second with a high K. value (0.9 MM). Growth of cells in hormone-depleted medium resulted in a two-to 3.5-fold increase in low K. 151D activity (P < 0.001). The addition of thyroid hormones to the culture medium resulted in a rapid, dosedependent inhibition of low K. 151) activity with the following order of analogue potency: rT3 2 T4> 3,5,3'-triiodothyronine (T3). Using serum-free culture conditions rT3 was -50 times more active than Tj. These inhibitory effects were noted within 15 min of hormone addition and could not be attributed to substrate competition with T4. These findings suggest that the control of T4 to T3 conversion by thyroid hormones in the anterior pituitary gland is mediated by a unique cellular mechanism that is independent of the nuclear T3 receptor, and under some circumstances, rT3 may play a regulatory role in controlling this enzymatic process.

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“…GH, cells are a rat pituitary cell line that produce growth hormone and prolactin and respond to physiological concentrations of L-triiodothyronine (T3) and L-thyroxine (1)(2)(3)(4). In medium supplemented with hypothyroid calf serum, T3 stimulates growth hormone synthesis (2,3) and inhibits prolactin production (2), and these responses appear to be initiated by a chromatin-associated cellular receptor (4)(5)(6).…”

mentioning

confidence: 99%

Thyroid and glucocorticoid hormones synergistically control growth hormone mRNA in cultured GH1 cells.

Shapiro¹,

Samuels²,

Yaffe³

1978

Proc. Natl. Acad. Sci. U.S.A.

160

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We have previously demonstrated that thyroid hormone controls growth hormone synthesis in GH1 cells and that the induction of the growth hormone response by glucocorticoid appears to be highly dependent on thyroid hormone action. Thyroid hormone induces growth hormone synthesis approximately 5-to 20-fold and cortisol increases this response 2-to 6-fold further. Long-term kinetics of the growth hormone response show that, without added thyroid hormone, cortisol can induce a small-growth hormone response after 48 hr of incubation. Sodium dodecyl sulfate/polyacrvlamide gel electrophoresis of proteins synthesized in intact celis demonstrates that the cortisol enhancement of growth hormone synthesis in cells incubated with thyroid hormone is a relatively selective process. Quantitation of growth hormone mRNA levels by cell-free protein synthesis demonstrates that the regulation of growth hormone synthesis by thyroid and glucocorticoid hormones is explained by a synergistic pretranslational control mechanism, presumably at the level of the growth hormone gene.

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Thyroid Hormone Action: A Cell-Culture System Responsive to Physiological Concentrations of Thyroid Hormones

Cited by 184 publications

References 26 publications

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Metabolic effect of 3,3',5'-triiodothyronine in cultured growth hormone-producing rat pituitary tumor cells. Evidence for a unique mechanism of thyroid hormone action.

Thyroid and glucocorticoid hormones synergistically control growth hormone mRNA in cultured GH1 cells.

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