17beta-estradiol modulates prostaglandin E2 release from human amnion-derived wish cells

Area of Science:

• Endocrinology
• Cell Biology
• Reproductive Biology

Background:

• Human amnion-derived WISH cells lack detectable estradiol-17beta binding sites.
• Cyclic adenosine monophosphate (cAMP) elevating agents can induce measurable binding sites.

Purpose of the Study:

• To investigate the modulation of prostaglandin E(2) (PGE(2)) release by 17beta-estradiol in WISH cells.
• To explore the role of cAMP in mediating estradiol-17beta's effects on WISH cells.

Main Methods:

• Treatment of WISH cells with 17beta-estradiol and cAMP-elevating agents (forskolin, Ro 20-1724).
• Measurement of [3H]estradiol-17beta binding.
• Assessment of prostaglandin E(2) release.
• Inhibition studies using tamoxifen, cycloheximide, and bovine serum albumin (BSA).

Main Results:

• 17beta-estradiol stimulates PGE(2) release in untreated cells but inhibits it in cells treated with Ro 20-1724.
• Both stimulatory and inhibitory effects are blocked by tamoxifen, cycloheximide, or when estradiol is bound to BSA.
• Estradiol increases cAMP levels in the presence of Ro 20-1724, suggesting cAMP mediates receptor availability and inhibition.

Conclusions:

• 17beta-estradiol modulates PGE(2) release in WISH cells via specific intracellular receptors, likely involving new protein synthesis.
• Cellular responsiveness to 17beta-estradiol is modulated by cAMP levels, which are influenced by the steroid hormone.
• Increased cAMP, induced by estradiol in the presence of Ro 20-1724, may enhance hormone receptor availability and inhibit PGE(2) release.