Abstract
To investigate the expression of endothelin-1 (ET-1) and endothelial nitric oxide (NO) synthase (eNOS) in normal and preeclamptic (PE) placentae. The present cross-sectional analytical study was performed in normal and PE primigravidae (n = 10 in each group) who were admitted to the North Okkalapa General and Teaching Hospital from February 2019 to February 2020. Serum samples were collected immediately before delivery, and placental tissues were collected immediately after emergency or elective cesarean section. The expression of placental eNOS was measured by western blot, and the levels of ET-1 in placental tissue homogenates and in the serum were measured by enzyme-linked immunosorbent assay (ELISA). The PE group had significantly higher serum levels of ET-1 (median: 116.56 pg/mL; IQR: 89.14-159.62 pg/mL) than the normal group (median: 60.02 pg/mL; IQR: 50.89-94.37 pg/mL) (p < 0.05). However, statistically significant differences were not observed in the levels of ET-1 in placental tissue homogenates between normal and PE placentae (median: 0.007 pg/µg of total protein; IQR: 0.002-0.0123 pg/µg of total protein; and median: 0.005 pg/µg of total protein; IQR: 0.003-0.016 pg/µg of total protein respectively). The median and IQR values of relative placental eNOS expression were significantly higher in the PE group than in the normal group (p < 0.05). The serum levels of ET-1 level were not significantly correlated with placental ET-1 expression, and neither there was a significant correlation between placental ET-1 and eNOS expression in any of the groups. The serum levels of ET-1 were significantly higher in PE pregnant women compared with normal pregnant women, while the ET-1 levels of placental tissue homogenates were not significantly different. Serum ET-1 rather than placental ET-1 might play a major role in the pathogenesis of PE.
Highlights
The central organ in the pathogenesis of preeclampsia (PE) is the placenta, and the only definitive cure is delivery
Serum ET-1 rather than placental ET-1 might play a major role in the pathogenesis of PE
Nitric oxide is synthesized from L-arginine, and it is catalyzed by a key enzyme called endothelial nitric oxide synthase,[2] and studies have investigated the association between the expression of placental eNOS and PE
Summary
The central organ in the pathogenesis of preeclampsia (PE) is the placenta, and the only definitive cure is delivery. Nitric oxide is synthesized from L-arginine, and it is catalyzed by a key enzyme called endothelial nitric oxide synthase (eNOS),[2] and studies have investigated the association between the expression of placental eNOS and PE. Smith-Jackson et al.[4] observed a significant increase in the mRNA expression of placental eNOS in preeclamptic pregnant women compared with normal pregnant women. Wang et al.[5] observed a significant reduction of eNOS expression in cultured endothelial cells from preeclamptic pregnant women compared with normal pregnant women. These associations are still controversial, and will remain the subject of active investigation
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