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Departments of Obstetrics and Gynecology, Pediatrics, Obstetrics and Reproductive Medicine (G.F., P.F., M.R., F.P.) and Pharmacology (L.M., C.N., D.C., G.G.), "Giorgio Segre," University of Siena, 53100 Siena, Italy; and Department of Gynecological Science and Reproductive Medicine (G.A.), University of Padua School of Medicine, 35100 Padua, Italy
Address all correspondence and requests for reprints to: Felice Petraglia, M.D., Chair of Obstetrics and Gynecology, Department of Pediatrics, Obstetrics, and Reproductive Medicine, University of Siena, Policlinico "Le Scotte," Viale Bracci, 53100 Siena, Italy. E-mail: petraglia{at}unisi.it.
Context: Preeclampsia (PE) is a disorder that occurs only during pregnancy. The placenta has a controlling role in this condition. Recent literature suggests that the oxidative stress is a component of PE and plays a main role in the link between decreased placental perfusion and the impaired function of maternal endothelium.
Objective: Because the human placenta expresses endothelin-1 (ET-1) and its circulating levels are high in pregnancies complicated with PE, the present study investigated the role of ET-1 on placental oxidative stress pathways.
Design: Human placental explants, JEG-3, and primary cytotrophoblast cells were cultured with increasing ET-1 concentrations for 6 and 24 h.
Setting: The study was conducted at tertiary clinical care centers in Siena and Padova, Italy
Interventions: Human placental explants, JEG-3, and primary cytotrophoblast cells were used to test ET-1 effect.
Main Outcome Measure(s): The main outcome measure was ET-1 mRNA and its receptor mRNAs, type A and B, detection by RT-PCR. The common markers of oxidative stress [malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), ascorbic acid (AA)] as well as cell proliferation and vitality were measured after stimulation periods.
Results: ET-1 inhibits cell proliferation and vitality and triggers oxidative stress in the human placenta by altering the balance between oxidant (increased MDA levels) and antioxidant (decreased GSH, GSSG, and AA) forces in favor of oxidation.
Conclusions: Because MDA damages endothelial cells, whereas GSH, GSSG, and AA protect them, we postulate that ET-1 may be one of the key links between primary placental disorders and the systemic endothelial dysfunction of PE.
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