Preeclampsia is a hypertensive disorder of pregnancy that is a leading cause of maternal and perinatal morbidity and mortality. The condition presents heterogeneously at varying gestational ages. Primary prevention for preeclampsia with low-dose aspirin is recommended for patients with clinical risk factors. Despite extensive research, there is no clearly defined pathophysiology for preeclampsia or treatment for preeclampsia besides delivery of the placenta. Delivery of patients with preeclampsia without severe features is indicated in the early term period at 37 weeks’ gestation and sooner if the patient develops severe preeclampsia. Management of preterm preeclampsia is guided by close assessment of the status of the pregnant woman and fetus, blood pressure control, and surveillance for any clinical progression to a more severe form of preeclampsia that may require preterm delivery. In a preterm gestation affected by preeclampsia, expectant management is intended to provide neonatal benefit though it does assume some maternal risk. Future research will hopefully further delineate the pathophysiology of the condition with the ultimate goal of finding a treatment to avoid associated morbidity and preterm delivery.
kinase 1 (sFLT1) in the supernatant of cell culture by enzyme-linked immunosorbent assay (ELISA), and transcription levels of sFLT1 and EDN1 (gene coding endothelin-1, ET-1) by qRT-PCR. RESULTS: After 4 hrs or 24 hrs of treatment, TNFa at doses of 10, 100 ng/ml significantly increased sFLT1 protein in the supernatant compared to controls (panel A & B in Fig. ). After 4 hrs, sFLT1 mRNAs were higher in cells treated with 10, 100 ng/ml of TNFa compared to controls (panel B in Fig.). After 24 hrs treatment, sFLT1 mRNAs were lower in cells treated with 100ng/ml of TNFa compared to controls while mRNA levels of sFLT1 in cells treated with 10 ng/ml TNFa were not different from those of controls (panel C in Fig.). TNFa at doses of 10, 100 ng/ml significantly increased EDN1 mRNA after 24 hrs treatment (panel E in Fig. ). CONCLUSION: TNFa exposure induces trophoblast production of anti-angiogenic factor sFLT1 and ET-1. sFLT1 may execute feedback inhibition on itself. The next step is to determine the effect of TNFa on trophoblast invasion.
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