Abstract
Pregnancy complicated by preeclampsia (PE) and intrauterine growth restriction (IUGR) promotes endothelial cell (EC) dysfunction. Our in vitro study aimed to evaluate the endothelial cell morphology after acute and chronic exposition to medium supplemented with serum taken from healthy pregnant women and women with IUGR and IUGR with PE. In the same condition, ECs viability, proliferation, reactive oxygen species (ROS) production, and serum concentration of vascular endothelial growth factor (VEGF) were also measured. Pregnant women with IUGR and IUGR with PE-delivered babies with reduced body mass and were characterized in elevated blood pressure, urine protein loss, and reduced level of VEGF. The 24 hours of exposition did not exert any morphological changes in ECs, except the reduction in cell viability, but prolonged exposition resulted in significant morphological changes concerning mostly the swelling of mitochondria with accompanying ROS production, cell autophagy, reduced cell viability, and proliferation only in complicated pregnancies. In conclusion, the sera taken from women with IUGR and IUGR with PE show a detrimental effect on ECs, reducing their viability, proliferation, and generating oxidative stress due to dysfunctional mitochondria. This multidirectional effect might have an adverse impact on the cardiovascular system in women with IUGR and PE.
Highlights
Preeclampsia is a hypertensive disease that complicates 2–8% of pregnancies characterized by high blood pressure and signs of damage to another organ system, most often the liver and kidneys
In this present paper, based on extensive medical reports that show endothelial cell (EC) dysfunction in intrauterine growth restriction (IUGR) and IUGR complicated with PE, we evaluated the morphological abnormalities in endothelium after being exposed to sera taken from pregnancies complicated with PE and PE with IUGR
No statistically significant relationships were obtained. The results of these analyses showed that the primary selection of patients into the studied groups could be supported, since the groups, especially IUGR and IUGR + PE, were not numerous
Summary
Preeclampsia is a hypertensive disease that complicates 2–8% of pregnancies characterized by high blood pressure and signs of damage to another organ system, most often the liver and kidneys. Roland et al describe many morphological changes of placental syncytium and their implications for the pathogenesis of this complex disorder [1,2] This pathological alteration promotes the increased release of soluble syncytial factors, including cytokines, eicosanoids, peroxides, the antiangiogenic factor-soluble fms-like tyrosine kinase (sFlt)-1, and soluble endoglin, as well as syncytiotrophoblast microparticles. These factors are suggested to promote maternal endothelial cells (ECs) dysfunction and are associated with placental damage in pregnancies complicated with intrauterine growth restriction (IUGR) [3,4]. Preeclamptic sera exerted diverse effects on ECs in vitro: (i) increased expression of fibronectin, (ii) had no impact on von Willebrand factor and tissue factor, (iii) decreased eNOS expression, (iv) increased inducible nitric oxide synthase (iNOS) expression, (v) augmented superoxide anion production, (iv) increased ECs permeability that was induced by IL-8 but not by eNOS [10,11,12]
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