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

孕产妇肥胖驱动的炎症和不良妊娠结局在先兆子痫小鼠模型中的作用

基本信息

批准号：
10333355
负责人：
Jennifer Liford Sones
金额：
$ 22.2万
依托单位：
LSU PENNINGTON BIOMEDICAL RESEARCH CTR
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-03-01 至 2025-01-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10333355
关键词：
Abnormal placentation Adipose tissue Adult Affect Angiogenic Factor Birth Weight Blood Pressure Blood Vessels Blood flow Body Weight decreased Body mass index Cell Count Cell Separation Cells Characteristics Clinical Conceptions Cytokine Gene Data Decidua Defect Development Disease Eating Eclampsia Embryo Etiology Event Exhibits Female Fetal Death Fetal Growth Retardation Fetus Gene Expression Genetic Models Goals Growth Health Hypertension Immune Impairment Inbreeding Infant Inflammation Inflammation Mediators Inflammatory Interleukin-6 Intervention Ischemia Laboratories Life Link Maternal Mortality Maternal-Fetal Exchange Measures Messenger RNA Metabolic Modeling Monitor Mothers Mus Natural Killer Cells Obesity Ovary PGF gene Pathogenesis Phenotype Physiological Placenta Placentation Play Population Pre-Eclampsia Pregnancy Pregnancy Outcome Premature Birth Prevalence Prevention Protein Tyrosine Kinase Proteinuria Recommendation Risk Risk Factors Role Signal Transduction Source Syndrome TNF gene Testing Thinness United States Uterus Vascular Endothelial Growth Factors Woman adverse outcome adverse pregnancy outcome angiogenesis attenuation cell type comorbidity cytokine early pregnancy experimental study fetal food surveillance gestational weight gain improved inflammatory milieu macrophage maternal hypertension maternal morbidity maternal obesity mortality mouse model offspring perinatal morbidity pregnancy disorder pregnancy hypertension pregnant prepregnancy prevent reproductive transcriptome sequencing

项目摘要

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.

项目摘要：怀孕是炎症的生理状态。但是，怀孕期间的炎症增加与不利的结果，例如先兆子痫（PE）。 PE的临床体征包括母体高血压和妊娠后半部分的蛋白尿。虽然PE在怀孕后期出现，但它的起源被认为是从怀孕开始，甚至在受孕之前开始。重要的是，孕产妇高血压仅在胎盘的输送；因此，普遍认为，异常胎盘在PE中起因果作用发病机理，尽管这是未知的病因。许多母体特征，包括肥胖症，是开发PE的已知风险因素。假设的母亲肥胖可能有助于增强炎症和随后的异常胎盘血管发育。这些的总体目标拟议的研究是检验以下假设：特定免疫细胞产生的促炎性介质在母体脂肪组织中，在母亲界面上减少了促血管生成因子。我们将进行我们的使用PE的BPH/5小鼠模型的研究。