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Relationship of receptor affinity to the modulation of thyroid hormone nuclear receptor levels and growth hormone synthesis by l tri iodo thyronine and iodo thyronine analogs in cultured gh 1 cells


Journal of Clinical Investigation 63(6): 1229-1240
Relationship of receptor affinity to the modulation of thyroid hormone nuclear receptor levels and growth hormone synthesis by l tri iodo thyronine and iodo thyronine analogs in cultured gh 1 cells
L-Triiodothyronine (L-T3) induces an increase in growth hormone [GH] synthesis and mRNA in cultured GH1 cells, a rat pituitary cell line. In addition to regulating the GH response, L-T3 elicits a time- and dose-dependent reduction in the level of its nuclear receptor, which is a direct function of the occupancy of the receptor binding site. This study compared the relative affinity of L-T3, triiodothyroacetic acid, D-triiodothyronine (D-T3) and L-thyroxine (L-T4) for the receptor with the induction of the GH synthesis and the ability of these compounds to elicit a reduction in thyroid hormone nuclear receptor levels. Triiodothyroacetic acid and D-T3 were specifically examined because the biologic effect of these compounds in the intact rat is significantly lower than predicted by their affinity for the receptor using isolated rat liver nuclei in vitro. In intact cells each compound demonstrated an excellent relationship between the relative receptor affinity, the induction of GH production and the concentration-dependent reduction in nuclear receptor levels. With the exception of D-T3, the relative affinity of iodothyronine was identical for the receptor using intact cells in serum-free media, or isolated GH1 cell nuclei in vitro. The apparent receptor affinity of D-T3 with intact cells was 5.5-fold lower than with isolated nuclei, which suggests a decrease in cell entry of D-T3 relative to the other iodothyronines. Quantitation of the [125I]iodothyronine associated with the receptor in GH1 cells after a 36 h incubation with L-125I-T4 was 90% L-T4 and 10% L-T3, which indicates that the major effect of L-T4 in GH1 cells is a result of intrinsic L-T4 activity. Studies with dispersed rat anterior pituitary cells demonstrated that L-T3 induces GH synthesis and elicits a reduction in nuclear receptor levels in the same fashion as GH1 cells. The observation that thyroid hormone influences dispersed rat pituitary cells in a fashion qualitatively similar to GH1 cells may have implications for the GH response of the somatotroph cell in vivo to different thyroidal states.


Accession: 006301138



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