Vascular endothelial growth factor receptor-1 (VEGFR-1) is essential for the normal development and function of the placenta. Defective placental vasculogenesis and trophoblast function may lead to
pre-eclampsia, a pregnancy-specific syndrome of
hypertension and
proteinuria. In order to study the association of
VEGFR-1 with the development of
pre-eclampsia, a cross-sectional study was carried out to evaluate the concentration of soluble
VEGFR-1 (sVEGFR-1) in 360 serum samples and to analyze the expression of membranous
VEGFR-1 in 40 placental samples of normal and pre-eclamptic pregnant women. Serum and placental samples at different gestational ages were collected from the Department of Obstetrics and Gynaecology, VMMC and Safdarjang Hospital, New Delhi. The serum levels of sVEGFR-1 and the expression of membranous
VEGFR-1 were estimated by
enzyme-linked
immunosorbent assay and immunohistochemistry, respectively. The serum levels of sVEGFR-1 were seen to be positively increased (p=0.0001) in patients with
pre-eclampsia at different gestational intervals as compared to the healthy pregnant women they were matched with. However, receiver operating characteristic (ROC) curve analysis showed a higher sensitivity (89.17%) and specificity (90.0%) in early onset (< or =34 weeks) in contrast with the late-onset (>34 weeks) pre-eclamptic group. Also, significant up-regulation of membranous
VEGFR-1 immunoreactivity was observed in all placental cells (syncytiotrophoblast, cytotrophoblast, endothelial cells and Hofbauer cells) of pre-eclamptic groups in both < or =34 weeks (p=0.0001) and >34 weeks (p=0.0001) as compared to the normal group. Elevated sVEGFR-1 serum levels and up-regulated membranous
VEGFR-1 expression in placenta denote abnormality in
VEGF-mediated function in all placental cells, and thus may contribute to etiopathogenesis of
pre-eclampsia. Nevertheless, this study also shows the possible diagnostic utility of sVEGFR-1 as a sensitive and specific
biomarker for the early onset (< or =34 weeks) of
pre-eclampsia.