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Objectives Preeclampsia (preE), a syndrome of hypertension and proteinuria in pregnancy, is thought to be initiated with alterations of placental function. Hypoxia and oxidative stress can lead to placental apoptotic signaling, which pass the placental barrier and leave persistent defect in the circulation of the offspring that may predispose to a pathological response later in life. We assessed apoptotic signaling in placentas and umbilical cords from patients with or without preE. We also evaluated the pregnancy outcomes. Methods In this study, we recruited 20 normal pregnant (NP) and 20 preE consenting patients in an IRB approved prospective study. Inclusion criteria of preE patients include blood pressure >140/90 and proteinuria >300 mg of protein/24 h urine. Samples of placenta and umbilical cord were collected after deliveries. Pro-apoptotic Bcl-2-associated X protein (Bax), anti-apoptotic Bcl-2 protein, caspase 9 and pro-inflammatory protein cyclooxygenase-2 (Cox-2) expression were assayed both by western blot and immunohistochemistry. The p38 MAPK phosphorylation was evaluated by western blot. Comparisons were performed using ANOVA with Duncan’s post-hoc test. Results The ratio of Bax/Bcl-2 expression (Placenta: 1.2 fold, Cord: 1.5 fold), Cox-2 (Placenta: 0.8 fold, Cord: 2.5 fold), Caspase 9 (Placenta: 1.5 fold, Cord: 1.8 fold), and p38 phosphorylation (Placenta: 1.5 fold, Cord: 1.7 fold) were up-regulated (p Conclusions Apoptotic signaling is augmented in preE which alters the intrauterine environment by modulating the pattern of hormonal signals and activating the detrimental cellular signaling that has been transported to the fetus. Disclosures M.M. Co: None. D. Leonard: None. L. Perger: None. V.P. Govande: None. M.R. Beeram: None. R.O. Jones: None. S.R. Allen: None. T.J. Kuehl: None. M.N. Uddin: None.