Endothelial microvesicles in peripheral blood of pregnant women with preeclampsia

BACKGROUND: Endothelial dysfunction is the leading pathogenetic factor of preeclampsia. The function of the endothelium may be reflected in its ability to form microvesicles, which are generated by cells through the regulated shedding of the plasma membrane. AIM: The aim of this study was to evaluate the endothelial microvesicles count in peripheral blood of women with normal pregnancy and pregnancy complications such as gestational arterial hypertension and severe preeclampsia. MATERIALS AND METHODS: This study included 72 individuals, of whom there were healthy non-pregnant women (n = 21), women with normal pregnancy (n = 20), pregnant women with gestational arterial hypertension (n = 24), and pregnant women with severe preeclampsia (n = 7). To isolate microvesicles from peripheral blood, the differential centrifugation method was used. Microvesicles were treated with antibodies to vascular endothelial growth factor receptors (VEGFR1, VEGFR2), CD41a, CD34, and CD31 conjugated to fluorochromes. The absolute and relative count of microvesicles, as well as the fluorescence intensity, were analyzed using a BD FACSCanto II cytofluorimeter. RESULTS: In normal pregnancy, the count of microvesicles with the VEGFR1+, VEGFR2+, CD31+, and CD34+ phenotype was increased compared to non-pregnant women. In gestational arterial hypertension compared to normal pregnancy, no differences were found in the endothelial microvesicles count and endothelial marker expression. In severe preeclampsia, the total microvesicles count and endothelial cell derived microvesicles count in the peripheral blood plasma decreased in comparison with normal pregnancy and gestational arterial hypertension. While the expression of endothelial markers such as VEGFR1, VEGFR2, and CD34 in microvesicles membranes in severe preeclampsia increased compared to normal pregnancy and gestational arterial hypertension. CONCLUSIONS: An increase in the endothelial microvesicles count in normal pregnancy may be associated with an increase in the vascular bed area due to placenta formation. A decrease in the endothelial microvesicles count in severe preeclampsia is associated with damage to the endothelium and disruption of its function. Increased expression of endothelial cell receptors on microvesicles in severe preeclampsia may reflect compensatory reactions of the endothelium during the above damage.