The role of maternal obesity-driven inflammation and adverse pregnancy outcomes in a mouse model of preeclampsia

项目总结： 怀孕是一种生理状态的炎症。然而，怀孕期间炎症的加剧与 不良后果，如先兆子痫(PE)。PE的临床症状包括母体高血压和 妊娠后半期的蛋白尿。虽然PE出现在怀孕后期，但它的起源被认为是 在怀孕早期，甚至在怀孕之前就开始了。重要的是，产妇高血压只有在以下情况下才能解决 胎盘的产生；因此，人们普遍认为胎盘异常在PE中起着因果作用。 发病机制，尽管其病因尚不清楚。一些母性特征，包括肥胖， 是发展PE的已知风险因素。据推测，母亲肥胖可能会导致身高增加 炎症和随后的胎盘血管发育异常。这些项目的首要目标是 拟议的研究是为了检验这样一种假设，即由特定的免疫细胞产生的促炎介质 在母体脂肪组织中，减少母胎交界处的促血管生成因子。我们将进行我们的 采用BPH/5小鼠PE模型进行研究。

Project Summary: 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.