Pregnancy is a physiological state of inflammation. However, heightened inflammation during pregnancy is linked to adverse outcomes, such as preeclampsia (PE). The clinical signs of PE include maternal hypertension and proteinuria during the second half of gestation. While PE presents later in pregnancy, its origins are thought to begin early in pregnancy or even before conception. Importantly, maternal hypertension only resolves after delivery of the placenta; therefore, it is widely accepted that abnormal placentation plays a causal role in PE pathogenesis, though the etiology of this is unknown. A number of maternal characteristics, including obesity, are known risk factors for developing PE. It is hypothesized maternal adiposity may contribute to heightened inflammation and subsequent abnormal placental vascular development. The overarching goal of these proposed studies is to test the hypothesis that pro-inflammatory mediators produced by specific immune cells within maternal adipose tissue reduce pro-angiogenic factors at the maternal-fetal interface. We will conduct our studies using the BPH/5 mouse model of PE.
Preeclampsia (PE) is a hypertensive disorder of pregnancy that affects up to 8% of women in the United States and can cause maternal death (~76,000/year) and infant loss (~500,000/year). PE has significant fetal co- morbidities, including intrauterine growth restriction (IUGR), which carries long-term health consequences for the offspring into adult life. Maternal obesity is a major risk factor for PE and a better understanding of this is necessary to prevent, predict and treat this life-threatening disorder of pregnancy.
