This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Mitchell, M. D. Articles by Sato, T. A. Search for Related Content PubMed PubMed Citation Articles by Mitchell, M. D. Articles by Sato, T. A. Related Collections Female Endocrinology

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.