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Ferret, S,Dockery, P,Harvey, BJ
2001
May
Molecular And Cellular Endocrinology
17 beta-Oestradiol stimulates capacitative Ca2+ entry in human endometrial cells
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()
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RL95-2 (human endometrium) capacitative calcium entry 17 beta-oestradiol non-genomic PROTEIN-KINASE-C INTRACELLULAR CALCIUM-CONCENTRATION RAT DISTAL COLON ESTROGEN-RECEPTORS STEROID-HORMONES PLASMA-MEMBRANE EPITHELIAL-CELLS STORE DEPLETION HUMAN-SPERM PROGESTERONE
176
77
84
Oestrogen plays an essential role in regulating growth and differentiation in the human endometrium which undergoes dynamic morphological and functional changes during the menstrual cycle in preparation for implantation. In this tissue, it has been suggested that intracellular calcium could be a key signal in transducing early responses to steroid hormones. Here, we have investigated the rapid effects of 17 beta -oestradiol on [Ca2+]i in a human endometrial cell line (RL95-2). Using confocal imaging microscopy, we show that physiological concentrations of 17 beta -oestradiol trigger rapid and transient increases in [Ca2+]i. Our results demonstrate that 17 beta -oestradiol-induced [Ca2+]i variations are critically dependent on calcium influx via lanthanum-sensitive calcium channels. Moreover, the 17 beta -oestradiol-induced Ca2+ influx is significantly increased by the depletion of intracellular stores by thapsigargin and decreased by chelerythrine chloride, an inhibitor of protein kinase C. These data indicate a non-genomic action of 17 beta -oestradiol to stimulate capacitative Ca2+ entry through store-operated calcium channels via a PKC-sensitive pathway. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
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