Iwashita M, Watanabe M, Setoyama T, Mimuro T, Nakayama S, Adachi T, Takeda Y, Sakamoto S
Maternal and Perinatal Center, Tokyo, Japan.
Placenta. 1992 May-Jun;13(3):213-21. doi: 10.1016/0143-4004(92)90036-s.
The effect of activation of calcium- and phospholipid-dependent protein kinase (protein kinase C) on human chorionic gonadotropin (hCG) release by cultured trophoblast cells was studied and a role of protein kinase C in the GnRH-mediated hCG release was also evaluated. Both GnRH and 1-oleoyl-2-acetylglycerol (OAG), a protein kinase C activator, stimulated hCG release after 3 h incubation in a dose-dependent manner with ED50 of 55 nmol/l and 4.0 nmol/l, respectively. A tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) also stimulated hCG release while two non-tumor-promoting compounds, phorbol and 4 alpha-phorbol, failed to stimulate hCG release. hCG release by maximal effective dose of GnRH (10 mumol/l) or OAG (1 mumol/l) was further stimulated when cells were incubated with same concentrations of GnRH and OAG. OAG-stimulated hCG release was completely inhibited by a protein kinase C inhibitor, H-7, with ID50 of 23 nmol/l while H-7 did not affect GnRH-mediated hCG release. These results indicate that GnRH-stimulated hCG release is not mediated by protein kinase C pathway, however, the secretion of hCG is also regulated by the mechanism that involves protein kinase C activation.
研究了钙和磷脂依赖性蛋白激酶（蛋白激酶C）激活对培养的滋养层细胞释放人绒毛膜促性腺激素（hCG）的影响，并评估了蛋白激酶C在促性腺激素释放激素（GnRH）介导的hCG释放中的作用。GnRH和蛋白激酶C激活剂1-油酰基-2-乙酰甘油（OAG）在孵育3小时后均以剂量依赖性方式刺激hCG释放，其半数有效剂量（ED50）分别为55 nmol/l和4.0 nmol/l。促肿瘤的佛波酯12-O-十四酰佛波醇-13-乙酸酯（TPA）也刺激hCG释放，而两种非促肿瘤化合物佛波醇和4α-佛波醇则未能刺激hCG释放。当细胞与相同浓度的GnRH和OAG一起孵育时，最大有效剂量的GnRH（10 μmol/l）或OAG（1 μmol/l）刺激的hCG释放进一步增加。蛋白激酶C抑制剂H-7完全抑制了OAG刺激的hCG释放，其半数抑制剂量（ID50）为23 nmol/l，而H-7不影响GnRH介导的hCG释放。这些结果表明，GnRH刺激的hCG释放不是由蛋白激酶C途径介导的，然而，hCG的分泌也受涉及蛋白激酶C激活的机制调节。
