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17ß-Estradiol Modulates Prostaglandin E₂ Release from Human Amnion-Derived WISH Cells¹

^a Department of Biology, Section of General Physiology, University of Ferrara, 44100-I Ferrara, Italy ^b Montell Italia, Centro Ricerche "G. Natta," 44100-I Ferrara, Italy

ABSTRACT

In human amnion-derived WISH cells [³H]estradiol-17ß binding sites are not detectable, but they become measurable in cells exposed to cAMP elevating agents such as forskolin or Ro 20-1724. In cells unexposed to these drugs, 17ß-estradiol stimulates prostaglandin (PG)E₂ release but exerts an evident inhibitory effect in cells exposed to Ro 20-1724. Both stimulatory and inhibitory actions are inhibited by the estrogen receptor antagonist, tamoxifen, by cell pretreatment with cycloheximide, or when the hormone is bound to BSA. Our data demonstrate for the first time that 1) 17ß-estradiol modulates PGE₂ release from WISH cells, interacting with specific intracellular receptors and probably evoking new protein synthesis, and 2) WISH cell responsiveness to 17ß-estradiol seems to be modulated by cAMP, whose levels are significantly increased by the steroid hormone in the presence of Ro 20-1724. The nucleotide is presumably responsible for the enhacement of hormone receptor availability and for the inhibition of PGE₂ release observed in the presence of Ro 20-1724.

FOOTNOTES

First decision: 12 September 2000.

¹ This work was supported by grants from Ministero dell'Università e della Ricerca Scientifica e Tecnologica (60%).

² Correspondence: Maria Enrica Ferretti, Department of Biology, Section of General Physiology, University of Ferrara, via Luigi Borsari 46, 44100-I Ferrara, Italy. FAX: 0532 207143; clm{at}dns.unife.it

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