Microvascular endothelial cells from preeclamptic women exhibit altered expression of angiogenic and vasopressor factors.

Abstract

Preeclampsia (PE) is a severe complication of pregnancy associated with maternal and fetal morbidity and mortality. The underlying pathophysiology involves maternal systemic vascular and endothelial dysfunction associated with circulating antiangiogenic factors, although the specific etiology of the disease remains elusive. Our aim was to investigate the maternal endothelium in PE by exploring the expression of genes involved with endothelial function in a novel platform of maternal primary endothelial cells. Adipose tissue was sampled at the time of caesarean section from both normal and preeclamptic patients. Maternal microvascular endothelial cells were isolated by tissue digestion and CD31 magnetic Dynabeads. Cell purity was confirmed by immunofluorescence microscopy and flow cytometry. Western analyses revealed VEGF activation of VEGF receptor 2 (VEGFR2) and ERK in primary cells. Quantitative PCR analyses revealed significantly altered mRNA levels of various genes involved with angiogenesis and blood pressure control in preeclamptic cells, including soluble fms-like tyrosine kinase-1, endoglin, VEGFR2, angiotensin receptor 1, and endothelin compared with cells isolated from normal pregnancies. Overall, maternal endothelial cells from preeclamptic patients exhibit extensive alteration of expression of factors associated with antiangiogenic and vasoconstrictive phenotypes, shedding light on the underlying mechanisms associated with the vascular dysfunction characteristic of PE.