Prostaglandin F2α and E1 regulation of proliferation in primary cultures of rabbit endometrial cells

✍ Scribed by David J. Orlicky; Rita Lieberman; L. E. Gerschenson

• Publisher: John Wiley and Sons
• Year: 1986
• Tongue: English
• Weight: 705 KB
• Volume: 127
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041270108

✦ Synopsis

The study of growth of endometrial cells is of importance in reproductive biology. Several factors and hormones are thought to play important roles in the control of growth. Prostaglandin F2<. (PGF2,J causes an increase in both tritiated thymidine ([3H]Tdr) incorporation into DNA and in t h e cell number of primary cultures of rabbit endometrial cells cultured in a serum-free, chemically defined media. Prostaglandins F1,,, El, E, , A,, and B2 and arachidonic acid (all tested at lo-' M) do not affect [?H]Tdr incorporation as compared to control cultures. The increase in [3H]Tdr incorporation into DNA in response to PGF2-stimulation is concentration-dependent (optimal -3 x lo-' M) and is seen starting -9 hr poststimulation. Both prostaglandin El (PGE1) and prostaglandin E2 (PGE,), but not PGs F,,,, I , , A,, B, , their parent molecules, or related molecules, antagonize and can completely block the PGF,,-induced increase in [3H]Tdr incorporation into DNA. This antagonism is seen both when the cells are pretreated with PGE, prior to the PGF,,, stimulation and when the cells are exposed to both PGEl and PGF2,, simultaneously, Exogenously added 8-Br-CAMP mimics the PGEl antagonism of PGF,,,. The PGF,,>-induced increase in H]Tdr inLorporation is not synergistic, antagonistic, or additive with the [ H]Tdr incorporation increase in response to either estradiol-17P or epidermal growth factor. The specific effect of PGF],, on primary culture endometrial cell growth and it5 antagonism by PGE1, PGE,, and 8-Br-CAMP are new findings.