Long-term effects of calcium availability on prolactin and protein synthesis in human decidual cells.

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.