Cole O F, Seki H, Sullivan M H, Elder M G
R.P.M.S. Institute of Obstetrics & Gynaecology, Hammersmith Hospital, London, UK.
Prostaglandins. 1995 Feb;49(2):69-77. doi: 10.1016/0090-6980(95)00006-v.
Basal prostaglandin E2 (PGE2) synthesis by human decidual cells was stimulated by phorbol myristate acetate (PMA) which activates protein kinase C. Staurosporine, which is an inhibitor of protein kinase C in most systems, also increased basal PGE2 synthesis. Further work is needed to explain this finding, as another inhibitor of protein kinase C, H7, inhibited PGE2 production under similar culture conditions. Interleukin-1 beta (IL-1 beta)-stimulated PGE2 synthesis was potentiated by coincubation with PMA or staurosporine, indicating that IL-1 beta and protein kinase C increase decidual PGE2 synthesis through different mechanisms. Desensitization of the decidual cells for 24 h with PMA did not affect IL-1 beta-stimulated PGE2 synthesis. The complex roles of protein kinase C in regulating decidual prostaglandin synthesis require further investigation, but it is clear that the effects of IL-1 beta are not mediated by protein kinase C.
佛波醇肉豆蔻酸酯乙酸酯（PMA）可刺激人蜕膜细胞合成基础前列腺素E2（PGE2），PMA可激活蛋白激酶C。在大多数系统中作为蛋白激酶C抑制剂的星形孢菌素，也增加了基础PGE2的合成。由于蛋白激酶C的另一种抑制剂H7在类似培养条件下抑制了PGE2的产生，因此需要进一步开展研究来解释这一发现。白细胞介素-1β（IL-1β）刺激的PGE2合成在与PMA或星形孢菌素共同孵育时得到增强，这表明IL-1β和蛋白激酶C通过不同机制增加蜕膜PGE2的合成。用PMA使蜕膜细胞脱敏24小时并不影响IL-1β刺激的PGE2合成。蛋白激酶C在调节蜕膜前列腺素合成中的复杂作用需要进一步研究，但很明显，IL-1β的作用不是由蛋白激酶C介导的。
