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-mediated rapid stimulation of Ca2+ levels and prolactin release in a pituitary cell line
1 Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, Texas, USA
* To whom correspondence should be addressed. E-mail: cswatson{at}utmb.edu.
The role of membrane estrogen receptor-
(mER) in rapid nongenomic responses to
17
-estradiol (E2) was tested in sublines ofGH3/B6 rat prolactinoma cells selected for
high (GH3/B6/F10) and low (GH3/B6/D9) mER expression. E2 elicited rapid,
concentration-dependent intracellular Ca2+ ([Ca2+]i) increases in the F10 subline. Lack
of inhibition by thapsigargin depletion of intracellular Ca2+ pools, together with
abrogation of the response in Ca2+-free medium, suggested an extracellular source of
Ca2+ for this response. The participation of voltage-dependant channels in the E2-
induced [Ca2+]i increase was confirmed by the specific L-type Ca2+ channel inhibitor
nifedipine. For comparison, the D9 mER-depleted subline was insensitive to steroid
action via this signaling mechanism. [Ca2+]i elevation was correlated with prolactin
(PRL) release in the F10 cell line in as little as 3 min. E2 caused a much higher PRL
release than KCl treatment (which caused maximal Ca2+ elevation), suggesting that
secretion was also controlled by additional mechanisms. Participation of mER in
these effects was confirmed by the ability of E2-peroxidase (a cell-impermeable analog
of E2) to cause these responses, blockage of the responses with ER antagonist ICI
182 780, and the inability of the E2 stereoisomer 17-E2 to elicit a response. Thus
rapid exocytosis of PRL is regulated in these cells by mER signaling to specific Ca2+
channels utilizing extracellular Ca2+ sources and additional signaling mechanisms.
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