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Identification of 9,11ß-Prostaglandin F₂ in Human Amniotic Fluid and Characterization of Its Production by Human Gestational Tissues

Liggins Institute (M.D.M., M.C.C., H.-Y.L., R.J.A.H., T.A.S.), University of Auckland, and National Research Centre for Growth and Development (M.D.M.), 1020 Auckland, New Zealand; and Perinatal Research Branch (T.C., R.R.), National Institute of Child Health and Human Development, Detroit, Michigan 48201

Address all correspondence and requests for reprints to: Professor Murray D. Mitchell, Liggins Institute, University of Auckland, 2-6 Park Avenue, Grafton, Auckland, New Zealand. E-mail: m.mitchell{at}auckland.ac.nz.

Context: 9,11ß-Prostaglandin F₂ (9,11ß-PGF₂) can contract uterine smooth muscle with a potency equal to PGF₂. Its presence in the human uterus and production by human gestational tissues is unknown.

Objective: These studies were performed to determine whether the PGD₂-derived 9,11ß-PGF₂ is both present in human amniotic fluid and synthesized by human gestational tissues and if so, whether labor-related substances could regulate its production.

Results: Detectable concentrations of 9,11ß-PGF₂ were found in amniotic fluid samples and appeared to increase in late gestation. All gestational tissues studied synthesized 9,11ß-PGF₂, with the placenta having the highest basal production rate, followed by the amnion and then the choriodecidua. IL-1ß and TNF caused concentration-dependent increases in 9,11ß-PGF₂ production in human amnion and choriodecidual explants. Moreover, treatment of choriodecidual and placental explants with lipopolysaccharide resulted in a significant increase in 9,11ß-PGF₂ production rates, reaching a maximum of 13-fold in the choriodecidua. Studies examining the effects of the addition of exogenous PGD₂ strongly indicated that the choriodecidua has significant ability to convert PGD₂ to 9,11ß-PGF₂, whereas the amnion has little.

Conclusions: These results demonstrate for the first time that 9,11ß-PGF₂ is present in human amniotic fluid and that it is produced by human gestational tissues and up-regulated by bacterial cell wall components and proinflammatory cytokines. We suggest that this prostaglandin may play a part in the mechanisms of human labor at term and preterm.