Introduction
Preeclampsia is a dangerous cardiovascular disorder of pregnancy and a leading cause of maternal and neonatal death globally. Although the pathogenesis is poorly understood, angiogenic imbalance is a hallmark feature. We aimed to elucidate the impact of angiogenic imbalance (high sFlt-1/low FKBPL) on the maternal cardiovascular system during pregnancy and to evaluate potential treatments in an established in vivo model1.
Methods
Wild-type (WT) and fkbpl+/- C57BL/6N mice were administered RALA-sFlt-1 (5μg) nanoparticles intravenously on embryo day (E)8 and 12 and randomly allocated to i) control (100μl, n=10), ii) exercise (n=5), iii) metformin (200 mg/kg/day via drinking water, n=7) or iv) AD-01 (0.003mg/kg/day, n=8). Blood pressure and heart rate were measured using the tail-cuff method every two days from E8. Echocardiography and placenta/embryo weight were determined, and tissues were harvested on E18 for analysis.
Results
Nanoparticles (sFlt1-RALA) showed satisfactory size (<100 nm), charge (40–60 mV), and excellent uniformity. In WT mice, pregnancy increased cardiac output vs. non-pregnant controls (p<0.0081). sFlt-1 overexpression reduced cardiac output vs. vehicle controls (p<0.044), while exercise restored it (p<0.0015) and metformin showed a trend toward improvement (p<0.054). In fkbpl+/- mice, exercise showed a trend toward rescuing sFlt-1-induced cardiac output reduction (p<0.065). At GD12, fkbpl+/- mice with sFlt-1 overexpression in the exercise group showed significant improvements in systolic (p<0.027), diastolic (p<0.031), and mean (p<0.028) arterial pressure, compared to sFlt-1 fkbpl+/- controls. ELISA showed a significant reduction in cardiac sFlt-1 protein in metformin-treated sFlt-1 fkbpl+/- mice (p<0.035). Uterine artery resistance and pulsatility indices were not significantly altered across treatment groups.
Conclusion
Our nanoparticle-induced preeclampsia model of angiogenic imbalance, driven by high sFlt-1 and/or low fkbpl expression, adversely impacts the maternal cardiovascular system. Exercise and metformin show therapeutic potential in reversing dysfunction, which is clearly fkbpl genotype dependent.