Abstract
Abstract: :
Purpose: Membrane steroid binding protein, which we identified in lens epithelial cells, is hypothesized to mediate a rapid effect of progesterone on lens calcium flux. The present result tests this hypothesis. Methods: We studied the effect of progesterone on Ca2+ signaling in in situ lens epithelial cells loaded with Fura-2 and fluorescence imaging system to evaluate the short-term effect of progesterone. The effect of progesterone on the calcium channel receptors was studied using Mn quenching technique. Results: Progesterone (10-100uM) induced a transient increase in [Ca2+]i within seconds, which is due to Ca2+ influx from the extracellular milieu, as shown by the effects of calcium chelator EGTA . Progesterone has no significant effect on the store-mediated release in the absence of extracellular Ca2+. Progesterone inhibited the thapsigargin-induced sustained [Ca2+]i elevation. It appears that progesterone reduces thapsigargin mediated calcium influx. A Mn2+-induced decline of fluorescent intensity at 360nm excitation was accelerated. However, in some cells, there was a transient decline in the rate of Mn2+ quench rate. Conclusion: This is the first report of a nongenomic rapid effects of a steroid hormone on lens cells and specifically on the intracellular concentration of calcium in lens epithelial cells. These data indicate a novel mode of direct action of progesterone on lens epithelial cells, which is not mediated through the classical nuclear receptor response, but likely through plasma membrane receptors.
Keywords: 338 cataract • 334 calcium • 541 receptors: pharmacology/physiology