Abstract
Recent clinical studies in pregnant women show an angiogenic imbalance present in a large fraction of women who go on to develop pre‐eclampsia (PE). These angiogenic factors include members of the vascular endothelial growth factor family, VEGF, PlGF, and the soluble form of their receptor: sFlt‐1. Similarily, soluble endoglin, an antagonist in the transforming growth factor β signaling pathway, has been recognized for its antiangiogenic potential. BPH/5 mice exhibit the cardinal symptoms of PE (late gestational hypertension, proteinuria) thus we hypothesized that an angiogenic imbalance would be found in BPH/5 mice. ELISA assays using plasma collected at early (d10.5–12.5), mid (d14.5) and late (d18.5) gestation revealed a decrease in circulating VEGF and PlGF in early gestation in BPH/5 mice (VEGF: 29.0±1.2 pg/ml vs. C57 84.1±15.3 pg/ml, n=3, p<0.05; PlGF:80.08±29.21pg/mL(BPH/5) vs. 418±58.29pg/mL (C57), n=4–5, p<0.05) and an elevated sFlt‐1 late in gestation (BPH/5:21.36±2.48 fold non‐pregnant (NP)state; C57:10.67±0.77 fold NP, n=6–7, p<0.01). Similarly, soluble endoglin levels are increased in BPH/5 mice at early gestation. These support the hypothesis that an angiogenic imbalance may underscore some of the pathological processes and demonstrate that BPH/5 is a good model to study in detail the role of angiogenic imbalance in PE.
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