Physiological Apoptotic Agents have Different Effects upon Human Amnion Epithelial and Mesenchymal Cells

• Published in: Placenta (Eastbourne) Vol. 24; no. 2-3; pp. 173 - 180
• Main Authors: Moore, R.M, Silver, R.J, Moore, J.J
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.02.2003; Elsevier
• Subjects: 8-Bromo Cyclic Adenosine Monophosphate - pharmacology; Adult; Amnion - drug effects; Amnion - metabolism; Amnion - pathology; Apoptosis - drug effects; Biological and medical sciences; Cell Line; Cyclooxygenase Inhibitors - pharmacology; Dinoprostone - metabolism; DNA Fragmentation - drug effects; Dose-Response Relationship, Drug; Epithelial Cells - drug effects; Epithelial Cells - metabolism; Epithelial Cells - pathology; Female; Fundamental and applied biological sciences. Psychology; Humans; Immunologic Factors - pharmacology; Lactosylceramides - pharmacology; Mesoderm - drug effects; Mesoderm - metabolism; Mesoderm - pathology; Mother. Fetoplacental unit. Mammary gland. Milk; Nitrobenzenes - pharmacology; Pregnancy; Pregnancy. Parturition. Lactation; Prostaglandin D2 - analogs & derivatives; Prostaglandin D2 - pharmacology; Pyrazoles - pharmacology; Sulfonamides - pharmacology; Vertebrates: reproduction; Human; Prostaglandin-endoperoxide synthase; Prostaglandin; Fetal membrane; Enzyme; Arachidonic acid derivatives; Transferases; Enzyme inhibitor; Mesenchyma; Metabolism; Protein kinase; Eicosanoid; Ceramide; Amnion; Epithelial cell; Female; Oxidoreductases; Apoptosis
• DOI: 10.1053/plac.2002.0886
• ISSN: 0143-4004

Foetal membrane rupture is thought to follow from gene-controlled tissue remodelling and apoptosis. We reported previously that staurosporine, cycloheximide, actinomycin D, as well as more physiological apoptotic agents (lactosylceramide, 15d-PGJ2) increase prostaglandin release in parallel with induction of apoptosis in WISH and amnion epithelial cells. Also, inhibition of prostaglandin release by cyclooxygenase inhibitors or PKA activators is accompanied by a parallel decrease in apoptosis. We hypothesize that amnion prostaglandin metabolism is linked with apoptosis in amnion epithelial cells and thus to membrane rupture. Amnion mesenchymal cells are also critical for membrane integrity. Their susceptibility to apoptotic agents is unknown and is the subject of this report. In amnion epithelial cells, lactosylceramide (125μm) induced 6.5-fold, 20-fold increases in PGE2 and NMP production (apoptosis), respectively. Conversely, in mesenchymal cells, lactosylceramide doses up to 200μm had no effect on PGE2 or NMP release. In both cell types, incubation with 15d-PGJ2 (5–100μm) demonstrated dose and time dependent increases in PGE2 and NMP. PKA activators inhibited 15d-PGJ2 induced PGE2 release and apoptotis in epithelial cells, but not in mesenchymal cells, however. Major amnion cell types have different sensitivities to physiological apoptotic agents. Prostaglandin release occurs coincident with apoptosis in both amnion epithelial and mesenchymal cells.