Couderc B, Dufy-Barbe L, Sartor P
Laboratoire de Neurophysiologie CNRS URA 1200, Université de Bordeaux 2, France.
Placenta. 1995 Sep;16(6):527-37. doi: 10.1016/s0143-4004(05)80004-9.
Ever since decidual cells were recognized as the source of decidual prolactin (dPRL), very few reports have dealt with the role of calcium (Ca2+) on dPRL synthesis and release. In a recent work, we described the presence of T-type Ca2+ channels in these cells, giving Ca(2+)-dependent action potentials. However, we failed to demonstrate any action of decidual cell Ca2+ modulation on acute dPRL release, but observed only long-term effects. We have now investigated these effects on decidual protein and dPRL synthesis after 24 h treatments. When Ca2+ channel blockers or EGTA (2 mM) were added to the culture medium, dPRL release and [3H] leucine incorporation into proteins decreased. Increasing external Ca2+ up to 2 mM instead of 0.8 mM or changing the external K+ concentration (30 mM instead of 5.6) had no consequence on dPRL release, whereas 2 mM of Ca2+ enhanced total protein synthesis. No toxicity was noted with these treatments. Finally a possible effect of Ca2+ modulation on dPRL synthesis was studied using [35S] methionine. The specific activity of [35S] methionine on dPRL was similar in control and treated cells (EGTA, 2 mM Ca2+, cobalt). These results support the idea that Ca2+ controls dPRL synthesis in decidual cells, acting only on general protein synthesis processes.
自从蜕膜细胞被确认为蜕膜催乳素（dPRL）的来源以来，很少有报告涉及钙（Ca2+）对dPRL合成和释放的作用。在最近的一项研究中，我们描述了这些细胞中存在T型Ca2+通道，可产生依赖于Ca2+的动作电位。然而，我们未能证明蜕膜细胞Ca2+调节对急性dPRL释放有任何作用，仅观察到长期影响。我们现在研究了24小时处理后这些因素对蜕膜蛋白和dPRL合成的影响。当向培养基中添加Ca2+通道阻滞剂或EGTA（2 mM）时，dPRL释放以及[3H]亮氨酸掺入蛋白质的量均减少。将外部Ca2+浓度提高到2 mM而非0.8 mM，或者改变外部K+浓度（30 mM而非5.6 mM）对dPRL释放没有影响，而2 mM的Ca2+可增强总蛋白合成。这些处理未观察到毒性。最后，使用[35S]甲硫氨酸研究了Ca2+调节对dPRL合成的可能影响。在对照细胞和处理过的细胞（EGTA、2 mM Ca2+、钴）中，[35S]甲硫氨酸对dPRL的比活性相似。这些结果支持了Ca2+控制蜕膜细胞中dPRL合成的观点，其仅作用于一般蛋白质合成过程。
