ObjectiveFailure of normal uteroplacental vascular development is the main pathologic finding in the development of preeclampsia. We investigated whether important angiogenic factors, vascular endothelial growth factor (VEGF)-A, angiopoietin (Ang)-1 and Ang-2 are associated with the development of severe preeclampsia.Study designWe included 16 patients with severe preeclampsia and 45 controls. Placental tissue was obtained and immediately stored at −70 °C after delivery. Total RNA was extracted from placental tissue and RT-PCR was done. Quantitative real-time PCR analysis was applied for evaluating mRNA expression of VEGF-A, Ang-1, and Ang-2. GAPDH was used as a control gene. Maternal and fetal cord blood were drawn, stored, and finally assayed for VEGF-A, Ang-1, and Ang-2 by ELISA. Mann-Whitney U test was applied for statistical analysis.ResultsPlacental mRNA expression of Ang-2 was significantly increased in severe preeclampsia than in control (p<0.05). VEGF-A and Ang-1 mRNA expression showed no difference between two groups. Fetal cord blood Ang-2 was increased significantly (p<0.05). Maternal Ang-2 level was increased with marginal significance (p=0.067). There was no difference in maternal and fetal serum levels of VEGF-A and Ang-1.ConclusionThese data suggest that Ang-2 play an important role in the development of preeclampsia. ObjectiveFailure of normal uteroplacental vascular development is the main pathologic finding in the development of preeclampsia. We investigated whether important angiogenic factors, vascular endothelial growth factor (VEGF)-A, angiopoietin (Ang)-1 and Ang-2 are associated with the development of severe preeclampsia. Failure of normal uteroplacental vascular development is the main pathologic finding in the development of preeclampsia. We investigated whether important angiogenic factors, vascular endothelial growth factor (VEGF)-A, angiopoietin (Ang)-1 and Ang-2 are associated with the development of severe preeclampsia. Study designWe included 16 patients with severe preeclampsia and 45 controls. Placental tissue was obtained and immediately stored at −70 °C after delivery. Total RNA was extracted from placental tissue and RT-PCR was done. Quantitative real-time PCR analysis was applied for evaluating mRNA expression of VEGF-A, Ang-1, and Ang-2. GAPDH was used as a control gene. Maternal and fetal cord blood were drawn, stored, and finally assayed for VEGF-A, Ang-1, and Ang-2 by ELISA. Mann-Whitney U test was applied for statistical analysis. We included 16 patients with severe preeclampsia and 45 controls. Placental tissue was obtained and immediately stored at −70 °C after delivery. Total RNA was extracted from placental tissue and RT-PCR was done. Quantitative real-time PCR analysis was applied for evaluating mRNA expression of VEGF-A, Ang-1, and Ang-2. GAPDH was used as a control gene. Maternal and fetal cord blood were drawn, stored, and finally assayed for VEGF-A, Ang-1, and Ang-2 by ELISA. Mann-Whitney U test was applied for statistical analysis. ResultsPlacental mRNA expression of Ang-2 was significantly increased in severe preeclampsia than in control (p<0.05). VEGF-A and Ang-1 mRNA expression showed no difference between two groups. Fetal cord blood Ang-2 was increased significantly (p<0.05). Maternal Ang-2 level was increased with marginal significance (p=0.067). There was no difference in maternal and fetal serum levels of VEGF-A and Ang-1. Placental mRNA expression of Ang-2 was significantly increased in severe preeclampsia than in control (p<0.05). VEGF-A and Ang-1 mRNA expression showed no difference between two groups. Fetal cord blood Ang-2 was increased significantly (p<0.05). Maternal Ang-2 level was increased with marginal significance (p=0.067). There was no difference in maternal and fetal serum levels of VEGF-A and Ang-1. ConclusionThese data suggest that Ang-2 play an important role in the development of preeclampsia. These data suggest that Ang-2 play an important role in the development of preeclampsia.