الفهرس 
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Abstract
The development of the placental villi during human early gestation requires branching of immature intermediate villous vessels. This process occurs before the establishment of a placental blood circulation in physiologic environment of low oxygen tension, which is known to stimulate cytotrophoblast proliferation, inhibit trophoblast invasion, and promote endothelial cell mitosis. Although the fetal and maternal circulations are physically separated, a failure of this branching development and deficits in intra-villous capillary proliferation are associated with inadequate invasion and deficits in intra-villous capillary proliferation are associated with inadequate invasion of the Uteroplacental spiral arteries by extra-villous trophoblasts in pregnancies complicated by preeclampsia and small for gestational age (SGA) newborn infants.
SGA pregnancies with poor umbilical artery end-diastolic blood flow have placentae with reduced angiogenesis and low capillary density. These observations suggest that, although physically dissociated, coordination of trophoblast and villous endothelial cell development, proliferation, invasion, and differentiation must occur during the early stages of placental development to ensure normal pregnancy outcome. This process appears to be directed by genes encoding locally angiogenic factors (e.g.: vascular endothelial growth factor [VEGF] and placental growth factor [PIGF]) that are regulated by cytokines, oxygen tension and mechanical stimuli.
However, there are other important factors that also regulate angiogenesis by antagonizing VEGF and PIGF; most important is sVEGFR-1. sVEGFR-1 is a 100 kd dimer, that is the soluble receptor for VEGF and PIGF. It is a secreted protein; s-splice variant of the vascular endothelial growth factor (VEGF) receptor , truncated from VEGFR-1 and has 53% sequence identical to it. sVEGFR-1 is the major antagonist for both VEGF and PIGF; it is antiangiogenic factor ,prominent expression of sVEGFR-1 has been identified in placenta, renal mesangial cells and monocytes as well as in malignant melanoma cells. And the aim of work in this study was to compare the difference in serum vascular endothelial growth factor receptor-1 in both preeclamptic and normotensive pregnant women, and its significance in the diagnosis of preeclampsia. sVEGFR-1 is the major antagonist for both VEGF and PIGF; it is anti-angiogenic factor ,prominent expression of sVEGFR-1 has been identified in placenta, renal mesangial cells and monocytes as well as in malignant melanoma cells. And the aim of work in this study was to compare the difference in serum vascular endothelial growth factor receptor-1 in both preeclamptic and normotensive pregnant women, and its significance in the diagnosis of preeclampsia.
The present study was conducted on one hundred subjects divided into three groups. Group I include 25 pregnant women with mild preeclampsia, ranging from 24-35 weeks of gestation. Group II enrolled 25 pregnant women with severe preeclampsia, also ranging from 24-35 weeks of gestation. While group III consists of 50 pregnant normotensive females ranging between 24-35 weeks of gestation.