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