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Binding and second messengers of prostaglandins F 2α and E 1 in primary cultures of rabbit endometrial cells
Author(s) -
Orlicky David J.,
Lieberman Rita,
Williams Cheryll,
Gerschenson L. E.
Publication year - 1986
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041270109
Subject(s) - intracellular , endogeny , stimulation , receptor , prostaglandin e , prostaglandin , cell culture , second messenger system , cell growth , biology , endocrinology , medicine , chemistry , biochemistry , genetics
Several factors and hormones are thought to play a role in the growth control of endometrial cells. We have shown that prostaglandin F 2α (PGF 2α ) is a growth factor for primary cultures of rabbit endometrial cells grown in serum‐free, chemically defined medium and that prostaglandin E 1 (PGE 1 ) antagonizes the PGF 2α induction of growth (Orlicky et al., 1986). [ 3 H]PGF 2α binds to whole cells in a time (optimal ∼30 min)‐ and temperature‐dependent (optimal 37°C), disassociable (90% disassociable within 30 min), saturable (Kd 1 = 4.9 × 10 −8 M, n 1 = 1.2 × 10 5 molecules/cell; Kd 2 = 2.6 × 10 −7 M, n 2 = 3.0 × 10 5 molecules/cell), and specific manner. [ 3 H]PGE 1 binds in a time‐dependent (optimal 25 min), disassociable (90% disassociable within 10 min), saturable (Kd = 6.4 × 10 −8 M, n = 1.2 × 10 5 molecules/cell), and specific manner. This specific binding of [ 3 H]PGF 2α and [ 3 H]PGE 1 is down‐regulatable by prior treatment of the cultures with unlabeled ligand, and up‐regulatable by prior treatment of the cultures with indomethacin to inhibit endogenous PG synthesis. Proteolytic enzyme treatment for 2 min reduces the specific binding of PGF 2α by 75%. PGE 1 stimulates intracellular cAMP synthesis and accumulation in a time (optimal 10 min)‐ and concentration (half‐maximal stimulation at 10 −6 M)‐dependent manner but has no effect on intracellular cGMP. PGF 2α has no effect on either intracellular cAMP or cGMP in this system. We describe here for the first time the analysis at a biochemical level of the interaction between two prostaglandins, antagonistic to each other in terms of growth regulation.