Datta M, Roy P, Banerjee J, Bhattacharya S
Department of Zoology, Visva-Bharati University, West Bengal, India.
J Endocrinol. 1998 Sep;158(3):319-25. doi: 10.1677/joe.0.1580319.
Blood samples collected from 29 women (aged between 19 and 35 years) during the luteal phase of the menstrual cycle (between days 18 and 23 of the cycle) showed that deficiency in thyroid hormone level is related to a decrease in progesterone (P4) secretion. To observe the effect of thyroid hormone on human ovarian luteal cells, 3,5,3'-triiodothyronine (T3; 125 ng/ml) was added to luteal cells in vitro. T3 significantly stimulated progesterone release (P < 0.01) from luteal cells and this could be blocked by cycloheximide, indicating a protein mediator for the T3 effect. The T3 stimulatory effect was inhibited by anti-T3 antibody suggesting specificity of T3 action. Addition of T3 caused a more than threefold increase in cellular protein synthesis which was inhibited by cycloheximide. Preparation of partially purified thyroid hormone-induced factor (TIF) (from peak II of Sephadex G 100 chromatography of T3-incubated cells), and its addition to luteal cell incubations caused a significant increase in P4 release (P < 0.05). Incubation with trypsin or treatment with heat destroyed the stimulatory effect of TIF on P4 release, indicating the proteinaceous nature of TIF. Purified thyroid hormone-induced protein. (TIP) from rat granulosa cells and fish ovarian follicles greatly stimulated P4 release from human luteal cells. These results suggest that T3 stimulation of P4 release from human luteal cells is not direct, but is mediated through a putative protein factor, which appears to be a protein conserved through evolution as far as its biological activity is concerned.
在月经周期的黄体期（周期的第18至23天）采集的29名女性（年龄在19至35岁之间）的血样显示，甲状腺激素水平不足与孕酮（P4）分泌减少有关。为了观察甲状腺激素对人卵巢黄体细胞的影响，将3,5,3'-三碘甲状腺原氨酸（T3；125 ng/ml）添加到体外培养的黄体细胞中。T3显著刺激黄体细胞释放孕酮（P < 0.01），这一作用可被环己酰亚胺阻断，表明存在一种蛋白质介质介导T3的作用。抗T3抗体抑制了T3的刺激作用，提示T3作用具有特异性。添加T3导致细胞蛋白质合成增加了三倍多，这一增加被环己酰亚胺抑制。制备部分纯化的甲状腺激素诱导因子（TIF）（来自T3孵育细胞的Sephadex G 100色谱的峰II），并将其添加到黄体细胞培养物中，导致P4释放显著增加（P < 0.05）。用胰蛋白酶孵育或加热处理会破坏TIF对P4释放的刺激作用，表明TIF具有蛋白质性质。从大鼠颗粒细胞和鱼卵巢卵泡中纯化的甲状腺激素诱导蛋白（TIP）极大地刺激了人黄体细胞释放P4。这些结果表明，T3对人黄体细胞释放P4的刺激作用不是直接的，而是通过一种假定的蛋白质因子介导的，就其生物学活性而言，这种蛋白质因子似乎是一种在进化过程中保守的蛋白质。
