We have reported that, in cultured GC cells, the stress of incubation at 41°C enhances thyroid hormone stimulation of growth hormone (GH) in a manner similar to the effects observed in a model of nonthyroidal disease in rats. Since glucocorticoids are potentially involved in stress responses both in vivo and in cell culture, we studied the role of glucocorticoid in the enhancement of (which are rat somatotrophic tumor cells) triiodothyronine (T3)-induced GH synthesis due to heat stress. Hydrocortisone addition increased T3-induced GH synthesis and GH mRNA content in cultured GC cells at both 37Γ and 41Γ. Depletion of glucocorticoid endogenous to serum supplement of the tissue culture medium did not prevent the enhancement of T3-induced GH synthesis that occurred during incubation at 41Γ. The levels and affinity of glucocorticoid cytosolic receptors were not enhanced during incubation at 41Γ. Lastly, no change in the sedimentation coefficient of the cytosolic glucocorticoid receptor or in its translocation into the nucleus occurred during incubation at 41Γ. Thus, the enhancement of T3-induced GH production in GC cells by heat stress appeared independent of the effect of glucocorticoids and not mediated through glucocorticoid receptors.
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