Suen C S, Wilk S
Endocrinology. 1987 Aug;121(2):770-5. doi: 10.1210/endo-121-2-770.
The effect of exposure of GH3 cells to T3 on the TRH-degrading enzymes pyroglutamyl peptidase I (EC 3.4.19.3) and prolyl endopeptidase (EC 3.4.21.26) was studied. T3 produced a dose-dependent increase in the specific activity of pyroglutamyl peptidase I after 3 days of exposure. The EC50 for T3 was 5 X 10(-10) M. The specific activity of prolyl endopeptidase was unaffected by exposure to T3. The increase in pyroglutamyl peptidase I activity was dependent upon the time of exposure of the cells to this hormone. A maximal effect occurred at 72 h. The stimulation of pyroglutamyl peptidase I by T3 was totally blocked by cycloheximide, indicating that this enzyme is induced in GH3 cells by T3. The effect of T3 on the two TRH-degrading enzymes was also studied in the ACTH-secreting cell line AtT20. T3 had no effect on these enzymes in the AtT20 cell, suggesting that the effect of T3 on pyroglutamyl peptidase I may be cell specific. These studies indicate that the induction of pyroglutamyl peptidase I by T3 may contribute to the negative feedback regulation of T3 levels.
研究了将生长激素瘤细胞系（GH3细胞）暴露于三碘甲状腺原氨酸（T3）对促甲状腺激素释放激素（TRH）降解酶焦谷氨酰肽酶I（EC 3.4.19.3）和脯氨酰内肽酶（EC 3.4.21.26）的影响。暴露3天后，T3使焦谷氨酰肽酶I的比活性呈剂量依赖性增加。T3的半数有效浓度（EC50）为5×10⁻¹⁰ M。脯氨酰内肽酶的比活性不受T3暴露的影响。焦谷氨酰肽酶I活性的增加取决于细胞暴露于该激素的时间。最大效应出现在72小时。T3对焦谷氨酰肽酶I的刺激作用被放线菌酮完全阻断，表明该酶是由T3在GH3细胞中诱导产生的。还在促肾上腺皮质激素分泌细胞系AtT20中研究了T3对这两种TRH降解酶的影响。T3对AtT20细胞中的这些酶没有影响，这表明T3对焦谷氨酰肽酶I的作用可能具有细胞特异性。这些研究表明，T3对焦谷氨酰肽酶I的诱导可能有助于T3水平的负反馈调节。
