Abstract
BackgroundAn imbalance between pro- and anti-angiogenic factors contributes to impaired trophoblast invasion during pregnancy, leading to failure of uterine spiral artery remodeling, blood vessel ischemia, and pre-eclampsia (PE). Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are expressed in both the placenta and maternal blood. The present study investigated correlations between serum and placental SEMA3B as well as CUL1 levels in late-onset PE.MethodsThis cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a P < 0.05 considered statistically significant.ResultsWhile elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (R = 0.620, P = 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.ConclusionAlteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.
Highlights
Pre-eclampsia (PE) is characterised by development of hypertension and proteinuria after 20 weeks of gestation or immediately after delivery [1]
The present study investigated whether there is a correlation between maternal serum and placental levels of semaphorin 3B (SEMA3B) and cullin 1 (CUL1) late-onset PE subjects
The present study investigated whether there is a correlation between maternal serum and placental levels of SEMA3B late – onset PE subject
Summary
Pre-eclampsia (PE) is characterised by development of hypertension and proteinuria after 20 weeks of gestation or immediately after delivery [1]. It affects approximately 2%–8% of all pregnancies and is one of the major causes of maternal and fetal morbidity and mortality [2]. PE can be classified as early- or late-onset, each presenting with a different etiology [3]. Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are expressed in both the placenta and maternal blood. The present study investigated correlations between serum and placental SEMA3B as well as CUL1 levels in late-onset PE
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